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Updated: 20 hours 39 min ago

Paracetamol use in pregnancy and infancy linked to child asthma

Wed, 10/02/2016 - 13:25

"Babies given paracetamol are nearly a third more likely to develop asthma," the Mail Online reports. 

The study the news is based on also found a link between maternal use of the painkiller in pregnancy, and childhood asthma.

Pregnant women are advised not to take medicines if possible, but paracetamol is recommended as the best option if painkillers are needed to reduce a fever, because there is little evidence it can cause harm to the baby. Paracetamol is also recommended if painkilling or temperature reduction medicines are needed for babies.

However, recent research has found a potential link between paracetamol and asthma. This study set out to investigate the link further.

The researchers found paracetamol was linked to childhood asthma, both in cases when it had been taken by the pregnant woman and by the young baby (less than six months old). The study estimated that infant exposure to paracetamol increased the asthma risk by 29% and exposure in pregnancy led to a 13% increase; though this estimate was borderline significant.

They also found that the reason for taking the medication did not affect the chances of asthma. This suggests the increased chance of asthma may be due to paracetamol, not to the illness it is used to treat.

The results of this study will probably need to be replicated in larger populations before official advice on paracetamol use in pregnancy and infancy are changed. 

Where did the story come from?

The study was carried out by researchers from the Norwegian Institute of Public Health, the University of Oslo and the University of Bristol and was funded by the National Institutes of Health, the Norwegian Research Council and the Norwegian Extra Foundation for Health and Rehabilitation. 

The study was published in the peer-reviewed International Journal of Epidemiology, on an open-access basis, meaning it is free to read online.

Most of the UK media reported the study's findings accurately, but as is so often the case, the headline writers overstated the findings. A link between paracetamol use and asthma has only been suggested, not proven.


What kind of research was this?

This is a cohort study, which is a good type of study for investigating links between factors – in this case, between taking paracetamol in pregnancy or infancy, and children developing asthma. However, cohort studies cannot prove that one thing causes another. They can only show there is a link, and investigate factors that may or may not have affected the results.


What did the research involve?

Researchers took information about 114,761 children born in Norway between 1999 and 2008, and analysed it to look for links between paracetamol use and childhood asthma at the ages of three and seven. 

They adjusted their figures to take account of the illnesses that paracetamol had been used to treat, and other factors that might have affected the results. They then calculated the relative risk (RR) of the child having developed asthma.

The researchers included data on:

  • 53,169 children who had information on asthma at age three
  • 25,394 at age seven
  • 45,607 who had records of whether or not they had been given asthma medications by age seven

Women in the study were asked about their own paracetamol use, and the reasons for it, at 18 and 30 weeks of pregnancy. When the child was six months old, the women were asked whether they had given paracetamol to the child, and if so what for.

The researchers checked whether the type of illness people took paracetamol for – pain, high temperature or chest infection/flu – had an effect on the child's chances of getting asthma. They also adjusted figures to take account of the mother's age, whether she had asthma, whether she smoked during pregnancy, antibiotic use, weight, education level and number of children.

They also looked for any effect from the father having taken paracetamol, or the mother having taken paracetamol when not pregnant. This is to see whether something else, such as the parents' attitudes to health and medicines, might affect the results.


What were the basic results?

About 28% of the children were born to mothers who had used paracetamol during pregnancy only, and 15% had taken paracetamol in the first six months of life only. A further 19% had been exposed to paracetamol both in the womb and in the first six months of life. A total of 5.7% of children had asthma at three years of age.

The researchers found "modest associations" between the use of paracetamol and childhood asthma, both for use during pregnancy and use by the child during the first six months of life.

Women who used paracetamol during pregnancy but did not give it to their infant were 13% more likely to have a child with asthma by age three (relative risk (RR) 1.13, 95% confidence interval (CI) 1.02 to 1.25).

A child was 29% more likely to have asthma at age three if the child had been given paracetamol before six months of age but was not exposed to it during the pregnancy (RR 1.29, 95% CI 1.16 to 1.45). While they were 27% more likely to have asthma with exposure during pregnancy and the first six months of life (RR 1.29, 95% CI 1.14 to 1.41). Results were similar for asthma at age seven.

The researchers said their results did not change when they adjusted them to take account of the reason for the medication. They found no link between the father's use of paracetamol or mother's use outside of pregnancy, and asthma in the child.


How did the researchers interpret the results?

The researchers say their study "is by far the largest study to provide evidence that prenatal and infant paracetamol exposures have independent positive associations with asthma development" – in other words, that the study found paracetamol was linked to a higher chance of getting asthma. 

They go on to say their findings "suggest that the associations cannot be fully explained" by other factors, such as the illness that the mother or baby was taking paracetamol for.

"Paracetamol is the most commonly used analgesic among pregnant women and infants, and uncovering potential adverse events is of public health importance," they say.



This study tells us more about a potential link between paracetamol and childhood asthma. Other studies have suggested that taking paracetamol in pregnancy, or giving it to babies, might increase the risk of the child getting asthma, but this study gives more detail.

One strong possibility before this study was published was that the problem was not paracetamol, but the reason for taking it – for example, that the baby's asthma was linked to the mother or baby having a chest infection, not to the medicine they took to relieve it. However, this study tests that possibility and finds that it cannot completely explain the link to paracetamol.

There are some weaknesses in the study. It relies on the mother's report of paracetamol use and whether their child has asthma, which might not be reliable. It is possible that women who decided to take paracetamol while pregnant might have been more ill than women who had that illness but didn't take medication, which might have affected the results. Another major limitation is that the study did not determine the amount or frequency that paracetamol was taken either by the mother or the infant, so we do not know how this might affect the risk.

However, it is a large study and the researchers carried out checks to make their findings as reliable as possible. While a cohort study can never confirm that one thing causes another, it does seem likely that there is a link between asthma and paracetamol.

It's important to remember that the relative increase in risk of asthma, especially for women taking paracetamol during pregnancy, is quite low. The researchers say that advice on paracetamol use for pregnant women and babies does not need to change as a result of their study.

Women in the UK are advised that paracetamol is the preferred choice to treat mild or moderate pain, or high temperature. They are advised to take paracetamol at the lowest effective dose, for the shortest possible time.

Babies can be given paracetamol to treat high temperature or pain if they are over two months' old. Check the packet or information leaflet for information about the correct dose.

Ibuprofen can be given for pain and fever in children of three months and over who weigh more than 5kg (11lbs) and, again, check the recommended dosage.

Links To The Headlines

Babies given paracetamol are nearly a THIRD more likely to develop asthma. Mail Online, February 10 2016

Pregnancy health warning: Paracetamol could cause asthma in unborn babies. The Sun, February 10 2016

Pregnant women who take paracetamol more likely to have babies with asthma. Daily Mirror, February 10 2016

Links To Science

Magnus MC,  Karlstad Ø, Håberg SE, et al. Prenatal and infant paracetamol exposure and development of asthma: the Norwegian Mother and Child Cohort Study. International Journal of Epidemiology. Published online February 9 2016

Categories: NHS Choices

New NICE guidelines on sun exposure warn 'tanning is unsafe'

Wed, 10/02/2016 - 10:00

"No safe way to suntan, new NICE guidance warns," BBC News reports. The guidelines, produced by the National Institute for Health and Care Excellence (NICE), also stresses the benefits of moderate sun exposure.

This will help prevent vitamin D deficiency; which is more common in the UK than many people realise. It is estimated that around one in five adults and older children (aged between 11 and 18) have low vitamin D status. The figure is around one in seven for younger children.


What are the risks of overexposure?

Sunlight contains ultraviolet A (UVA) and ultraviolet B (UVB) radiation, both of which can be harmful to the skin. (The guidelines do not discuss artificial sources of UV light, such as sunbeds, but these are also thought to be harmful).

Risks of overexposure to sunlight include:

Non-melanoma is a leading cause of disfigurement, with an estimated quarter of a million cases occurring each year in the UK. Melanoma is a leading cause of cancer deaths in younger adults. More than 2,000 people die every year in the UK from melanoma.

Overexposure can also cause premature ageing of the skin, which can lead to signs and symptoms, such as :

  • dryness
  • itching
  • wrinkling
  • enlarged blackheads
  • loss of skin elasticity


At-risk groups

Groups of people particularly vulnerable to overexposure include:

  • children (particularly babies) and young people
  • people who tend to burn rather than tan
  • people with lighter skin, fair or red hair, blue or green eyes, or who have lots of freckles
  • people with many moles
  • people who are immunosuppressed (that is, they have less resistance to skin problems as a result of a disease or use of particular drugs)
  • people with a personal or family history of skin cancer (even if their natural skin colour is darker than that of the family member who had cancer)
  • outdoor workers
  • those with outdoor hobbies, for example, sailing or golf
  • people who sunbathe
  • people who take holidays in sunny countries


Preventing overexposure Avoid strong sunlight

Avoid spending long periods of time in strong sunlight. The sun is at its strongest from 11am to 3pm from March to October. It can also be very strong and have potentially damaging effects at other times. Even if it is cool or cloudy, it is possible to burn in the middle of the day in summer.

Wear suitable clothing

Skin should be protected from strong sunlight by covering up with suitable clothing, finding shade and applying sunscreen.

Suitable clothing includes:

  • a wide-brimmed hat that shades the face, neck and ears
  • a long-sleeved top
  • trousers or long skirts in close-weave fabrics that do not allow sunlight through
  • sunglasses with wraparound lenses or wide arms with the CE Mark and European Standard EN 1836:2005
Use sunscreen

When buying sunscreen, make sure it's suitable for your skin and blocks both ultraviolet A (UVA) and ultraviolet B (UVB) radiation.

The sunscreen label should have:

  • the letters "UVA" in a circle logo and at least 4-star UVA protection
  • at least SPF15 sunscreen to protect against UVB

Most people do not apply enough sunscreen. The amount of sunscreen needed for the body of an average adult to achieve the stated sun protection factor (SPF) is around 35ml or six to eight teaspoons of lotion.

If sunscreen is applied too thinly, the amount of protection it gives is reduced. If you're worried you might not be applying enough SPF15, you could use a stronger SPF30 sunscreen.

If you plan to be out in the sun long enough to risk burning, sunscreen needs to be applied twice:

  • 30 minutes before you go out
  • just before going out

Sunscreen should be applied to all exposed skin, including the face, neck and ears (and head if you have thinning or no hair), but a wide-brimmed hat is better.

Water-resistant sunscreen is needed if sweating or contact with water is likely.

Sunscreen needs to be reapplied liberally, frequently and according to the manufacturer's instructions. This includes applying straight after you've been in water (even if it is "water-resistant") and after towel drying, sweating or when it may have rubbed off.

Advice for babies and children

Take extra care to protect babies and children. Their skin is much more sensitive than adult skin, and repeated exposure to sunlight could lead to skin cancer developing in later life.

Children aged under six months should be kept out of direct strong sunlight.

From March to October in the UK, children should:

  • cover up with suitable clothing
  • spend time in the shade (particularly from 11am to 3pm)
  • wear at least SPF15 sunscreen

To ensure they get enough vitamin D, children aged under five are advised to take vitamin D supplements even if they do get out in the sun. Find out about vitamin D supplements for children.

Avoid tanning

There is no healthy way to tan. Any tan can increase your risk of developing skin cancer. Getting a tan does very little to protect your skin from the harmful effects of the sun. The idea that there is such a thing as a healthy tan is a myth.

The British Association of Dermatologists advises that people should not use sunbeds or sunlamps.

Sunbeds and lamps can be more dangerous than natural sunlight, because they use a concentrated source of ultraviolet (UV) radiation.

UV radiation can increase your risk of developing melanomas. Sunbeds and sunlamps can also cause premature skin ageing.

If you do want browner looking skin then fake tan is the way to go.


Sunlight and vitamin D

Vitamin D is essential for healthy bones, and we get most of ours from sunlight exposure.

We need vitamin D to help the body absorb calcium and phosphorus from our diet. These minerals are important for healthy bones and teeth.

A lack of vitamin D – known as vitamin D deficiency – can cause bones to become soft and weak, which can lead to bone deformities. In children, for example, a lack of vitamin D can lead to rickets. In adults, it can lead to osteomalacia, which causes bone pain and tenderness as well as muscle weakness.

Most people can make enough vitamin D from being out in the sun daily for short periods with their forearms, hands or lower legs uncovered and without sunscreen from March to October, especially from 11am to 3pm.

A short period of time in the sun means just a few minutes – about 10 to 15 minutes is enough for most lighter-skinned people – and is less than the time it takes you to start going red or burn. Exposing yourself for longer is unlikely to provide any additional benefits.

People with darker skin will need to spend longer in the sun to produce the same amount of vitamin D.

Groups of people who have little or no exposure to the sun for cultural reasons or because they are housebound or otherwise confined indoors for long periods, may be vitamin D deficient and may benefit from vitamin D supplements.

How long it takes for your skin to go red or burn varies from person to person. Cancer Research UK has a useful tool where you can find out your skin type, to see when you might be at risk of burning.

Vitamin D and pregnancy

Pregnant and breastfeeding women should take a vitamin D supplement to make sure their own needs for vitamin D are met, and their baby is born with enough stores of vitamin D for the first few months of its life.

You can get vitamin supplements containing vitamin D free of charge if you are pregnant or breastfeeding, or have a child under four years of age and qualify for the Healthy Start scheme.

Read more about vitamins and supplements in pregnancy

Links To The Headlines

No safe way to suntan, new NICE guidance warns. BBC News, February 9 2016

Don't go out in the sun for over 10 minutes warn health chiefs: Sunseekers told there is no such thing as a healthy tan as they are urged to slap on EIGHT teaspoons of sunscreen. Daily Mail, February 9 2016

No such thing as a safe tan, warn health officials. The Daily Telegraph, February 9 2016

Millions of British sun-worshippers warned there is "no safe way" to get a tan. Daily Mirror, February 9 2016

There's no safe way to get a natural sun tan, says official health guidelines. The Independent, February 9 2016

Categories: NHS Choices

'Bionic spine' could pave the way for new paralysis treatments

Tue, 09/02/2016 - 15:30

"'Bionic spine' could enable paralysed patients to walk using subconscious thought," reports The Guardian.

In a study using sheep, Australian researchers have developed a device that can record movement signals from the brain. It's hoped this will eventually lead to these signals being transmitted to other parts of the body.

The spine – specifically, the spinal cord – is essentially a signal cable. It transmits electrical impulses from the brain to other parts of the body. Damage to the spine can result in paralysis.

Restoring this signal process in humans has been described as the "Holy Grail" of bionic medicine, which uses technology and engineering to improve or restore bodily functions.

The researchers implanted the device, called a stentrode, via a blood vessel in the neck and guided it into position in a blood vessel overlying the part of the sheep's brain responsible for movement.

They found the device was able to record signals as the sheep moved around for a period of up to 190 days. These recordings were comparable to the recordings taken from electrodes implanted directly on to the brain.

Accurate recordings may mean this device can be used for people with paralysis to control bionic limbs and exoskeletons in the future.

While this technology is exciting, the usual caveats about early-stage research apply.

The first tests in humans are planned for 2017, and the results will give more of an indication about whether the device could be effective if implanted in humans – and, importantly, whether it would be safe.  

Where did the story come from?

The study was carried out by researchers from a number of institutions, including the University of Melbourne and the University of Florida, and was funded by grants from the US Defense Advanced Research Projects Agency (DARPA) Microsystems Technology Office, the Office of Naval Research (ONR) Global, and a National Health and Medical Research Council of Australia (NHMRC) Project Grant and Development Grant.

It was published in the peer-reviewed Nature Biotechnology.

The UK media has not reported the technical details and findings of this animal study at length, but the implications of the findings and the direction for future research has been discussed appropriately.   

What kind of research was this?

This was an animal study where a type of device or stent able to record brain activity (stentrode) was positioned in a blood vessel overlying the motor cortex. This is the part of the brain responsible for muscular activity.

This type of study is useful for the first testing stages of new devices or technologies, but it is not certain these findings will be replicated in humans.

However, the researchers did look for an animal model with blood vessel structures in the brain similar – but not identical – to humans, eventually settling on sheep.   

What did the research involve?

The researchers used human samples to investigate blood vessel structures in the human brain, and chose an animal model considered to have a comparable structure to human vessels. 

The stentrode, or "bionic spine", is a small device fitted with electrodes that can detect signals coming from the motor cortex.

Usually, inserting a device into the brain would require advanced brain surgery to open the skull, which carries the obvious risks of complications, such as postoperative infection.

However, in this study the device was inserted via a blood vessel in the sheep's neck, and was then guided under imaging through a thin tube called a catheter to its target position in a blood vessel overlying the motor cortex in the brain.

This could then record signals for movement. The movement signals coming from the device were validated by comparing them with electrodes implanted on to the brain surgically. 

What were the basic results?

In brief, the researchers were able to successfully position the stentrode within a blood vessel overlying the motor cortex of the brain, and record brain signals coming from freely moving sheep for a period of up to 190 days.

The content of these recordings was comparable to the recordings taken from electrodes implanted directly into the brain.  

How did the researchers interpret the results?

The researchers concluded that stentrodes may have wide-ranging applications in the treatment of a range of brain conditions. 


This early-stage study was conducted in sheep, and aimed to test whether a stentrode could be inserted into a blood vessel overlying the brain using a non-surgical method. Researchers then wanted to see whether the device was able to accurately record movement signals.

Overall, the results were promising. Implanting devices into the brain normally requires surgery to open the skull, which carries the associated risks of trauma, infection and inflammation. Also, devices positioned in brain tissue can be rejected by the immune system.

However, this device could be inserted through a blood vessel in the neck, and was successfully guided into the correct position in a blood vessel overlying the brain. As the results demonstrated, it was then able to record brain signals. 

The hope is this device could be used in the future for people with a spinal cord injury – such as those with paralysis – to control bionic limbs and exoskeletons with thought alone.

These signals are still present in the brain, but cannot be transmitted to the limbs. The stentrode would in effect bypass this problem, which is why it has been referred to as the "bionic spine".

A sheep model was used to replicate the structures found in humans as closely as possible. The stentrode technology used is currently in clinical use, which should allow easy transfer from animal models to humans.

However, the sheep used in this study weren't paralysed, so the big test now is whether these signals can actually be transferred into movement instructions.

The Guardian reported the researchers are now set to trial this device in humans at the Austin Health spinal cord unit. The device will similarly be inserted via one of the neck veins and, once implanted, will feed brain signals to another device positioned at the person's shoulder.

This will then translate signals into commands, which will be fed to the bionic limbs using Bluetooth wireless technology to tell them to move.

This technology is exciting and could provide hope for people with a spinal cord injury. But the research is still in its very early stages, and it is too soon to know when, or if, it will become available.

The researchers have planned the first tests in humans next year, and the results will give more of an indication about whether the device could be effective – and safe – in humans. 

Links To The Headlines

'Bionic spine' could enable paralysed patients to walk using subconscious thought. The Guardian, February 8 2016

Australia scientists develop 'bionic spine' which could help paralysed patients walk. The Daily Telegraph, February 9 2016

Tiny 'bionic spine' device that could help paralysed patients walk again WITHOUT brain surgery is hailed as a 'major breakthough'. Daily Mail, February 9 2016

Links To Science

Oxley TJ, Opie NL, John SE, et al. Minimally invasive endovascular stent-electrode array for high-fidelity, chronic recordings of cortical neural activity. Nature Biotechnology. Published online February 8 2016

Categories: NHS Choices

Hope that blood test 'could diagnose five types of cancer'

Mon, 08/02/2016 - 13:30

"A new blood test that detects five different forms of cancer is one step closer to becoming a reality and could save millions of lives around the world," the Mail Online reports. The test looks for abnormal changes in DNA – what is described as a DNA signature.

This laboratory research looked at ways to identify tumour DNA – DNA affected by abnormal cell growth – in blood samples and distinguish it from normal cellular DNA.

The researchers used tissue samples from five cancers – womb, lung, stomachcolon and breast tumours – and compared it with normal healthy tissue.

In brief, they found they could identify the cancerous tissue from a particular DNA signature around a certain gene (ZNF154).

Their tests reveal this test could be fairly accurate at detecting cancer at a concentration of 1% tumour DNA on a background of 99% normal DNA in a blood sample.  

There are many things to consider before any new screening or diagnostic test for cancer is introduced, especially with a "blanket screen" like this.

These issues include how and whether the test improves on current screening or diagnostic methods, as well as looking at the possible harmful effects, such as getting an incorrect positive screen result when you're in fact cancer free, or getting an incorrect negative screen result when you have cancer.  

Where did the story come from?

This study was carried out by researchers from the National Human Genome Research Institutes in the US, and published in the peer-reviewed Journal of Molecular Diagnostics.

The researchers report no sources of financial support and no conflicts of interest.

The Mail Online's reporting of the study is accurate, although its claim that, "a new blood test … could save millions of lives around the world" is prematurely optimistic: this research is in its early stages and has not been tested at a significant population level.

The Daily Telegraph's headline is slightly more restrained: "Blood test to spot five deadly cancers could prevent thousands of deaths". 

What kind of research was this?

This laboratory study examined a possible way of detecting DNA markers for cancer. The researchers report that work on cancer prevention, early diagnosis and treatment has reduced overall cancer death rates by 20% over the past 20 years.

Further advances in screening and diagnosis are, they say, where improvements in survival rates are likely to come. In many cases, the earlier a cancer is diagnosed, the better the outcome tends to be.

Tests that are able to detect genetic information coming from cancerous cells are a possible area for development. Previous research has shown how DNA from a tumour can be found freely circulating in the blood or in saliva, urine and stool samples, for example.

One approach is to look for what is called DNA methylation. This is a signalling method that controls gene activity in a cell, and genes are effectively "switched off".

There are a few specific cancer tests that have already been developed that involve detecting DNA methylation – for example, detecting specific genetic markers for lung cancer in lung fluid, or bowel cancer in stool samples. However, this is still an area of development.

This study builds on the researchers' previous work, where they identified a possible hypermethylation signal near a particular human gene (ZNF154).

This signal was found to come from ovarian and womb cancers and may be found in other cancers, too. This study measured the ZNF154 methylation signal across five different cancers. 

What did the research involve?

The researchers examined cell samples from womb, lung, stomach, colon and breast tumours, and comparison samples of normal tissues from the same organs.

In total, they examined 184 tumour samples and 34 normal tissue samples. They used complex laboratory techniques to analyse cancerous DNA methylation patterns and examine them on a background of normal DNA methylation patterns.      

The researchers then used their findings to identify possible classification methods that could be used in cancer screening. They looked at different ways to characterise methylated bases – the "letters" of DNA (A, C, G and T) – and identified features that could be used to distinguish cancerous tissue from normal tissue.

They then used computational simulation to indicate how reliable these features could be for classifying samples as tumours or normal tissue at various concentration levels, given that in a blood sample, for example, tumour DNA may be present at quite dilute levels.   

What were the basic results?

The researchers found all of the tumour types tested demonstrated hypermethylation at the ZNF154 gene site compared with the normal tissue.

The classification method with the best performance had almost perfect accuracy for distinguishing between normal and cancerous tissue.

Their computational simulation indicated circulating tumour DNA could be detected at a dilution of only 1% tumour DNA on a background of 99% normal DNA. 

How did the researchers interpret the results?

The researchers concluded their findings "suggest that hypermethylation of the ZNF154 [gene site] is a relevant biomarker for identifying solid tumour DNA and may have utility as a generalisable biomarker for circulating tumour DNA". 


This is very early-stage laboratory research that aimed to explore new avenues that could detect and diagnose cancer earlier – and hopefully ultimately lead to earlier and more successful treatment, and so better cancer survival rates. 

The study indicates taking blood samples and detecting DNA methylation from tumours could be one possible early screening or diagnostic method, and shows this technique's use for indicating womb, lung, stomach, colon and breast tumours.

However, there are likely to be many more stages of research necessary to build on these findings and check how reliable the test could be for different subtypes of these cancers, and also whether it could be used for other types of cancer.

Even then, there are many things to be taken into account before considering introducing any new screening or diagnostic test for cancer, including how and whether it improves on current screening or diagnostic methods.

For example, the media has highlighted the benefits of a blood test being "non-invasive", but current screening tests for bowel and breast cancer – taking stool samples and using mammograms, for instance – are also non-invasive.

Possible harmful effects also need to be considered, such as getting an incorrect positive screening result when you're in fact cancer free (false positive), or getting an incorrect negative screen result when you do have cancer (false negative). There is also the question of whether screening for certain cancers could seem to lead to improved survival time.

While early diagnosis often leads to a better prognosis, this is not the case for all cancers. Some people, for example, may face the emotional trauma of living with the knowledge that they have cancer for longer, but there still isn't an effective treatment to cure them.

In this situation, longer survival time might not actually mean better survival – it just means longer survival with a cancer diagnosis.

Ultimately, screening for any disease is no magic bullet, especially a potential "blanket screen" like the method outlined in this study.

Links To The Headlines

New blood test could diagnose FIVE different cancers 'without the need for invasive biopsies, saving millions of lives'. Mail Online, February 5 2016

Blood test to spot five deadly cancers could prevent thousands of deaths. The Daily Telegraph, February 5 2016

Links To Science

Margolin G, Petrykowska HM, Jameel N, et al. Robust Detection of DNA Hypermethylation of ZNF154 as a Pan-Cancer Locus with in Silico Modeling for Blood-Based Diagnostic Development. The Journal of Molecular Diagnostics. Published online February 5 2016

Categories: NHS Choices

Could statins treat common cause of vision loss?

Fri, 05/02/2016 - 12:00

"Statins could be miracle cure for blindness," reports the Express, following a new study into dry age-related macular degeneration (AMD), one of the leading causes of blindness in adults.

AMD is a condition caused by damage to part of the back of the eye called the macula. It’s called "dry" or "wet", depending on whether fragile blood vessels have developed to try to repair the damage. There are treatments for wet AMD, but none for the much more common dry form.

After promising results in the case of a single 63-year-old man, the researchers gave a high-dose of daily statin (80mg atorvastatin) over a year to 23 adults over 50. Ten of the group experienced some vision improvement and a reduction in fatty deposits called drusen in their eyes, but vision in the remaining 13 patients continued to get worse.

The study had several limitations, but this is understandable, given the early stage of this research. Most notably:

  • the study was very small
  • treatment was non-randomised
  • treatment was not concealed (blinding), so people knew what they were taking and why
  • there was no control group, so the results weren't compared to people taking no medication or "dummy" medication (placebo)
  • vision improvements reported by some participants might have been due to chance

The researchers also point out that dry AMD can vary a lot between people, so it's unlikely that statins would be effective for everyone with the condition.

Overall, there were signs that statins improved vision in dry AMD, but it didn't work for most people. It's not possible to know whether statins could be a "cure" for AMD without more research.

Where did the story come from?

The study was carried out by researchers from Harvard Medical School and the University of Crete, and was funded by Yeatts Family Foundation, the Mass Eye and Ear Neovascular AMD funds, the Loefflers Family Foundation, and the Research to Prevent Blindness Foundation.

The study was published in the peer-reviewed science journal EBioMedicine, and is free to read online.

Generally, the media over-inflated the results and didn't discuss the numerous and important limitations of this research.

Much of the coverage suggested statins may be the miracle cure for blindness in general. However, the study was specifically targeting a particular type of vision loss and potential blindness: dry AMD with large soft drusen deposits.

Other types of dry AMD exist, as well as wet AMD. The researchers themselves said that it is unlikely that statins will be effective across the broad range of dry AMD, as the condition is quite variable.

What kind of research was this?

This was an open-label, small prospective study looking at the effects of high-dose statins on progression of dry AMD.

Small studies like this are useful to test a hypothesis – in this case, that high-dose statins might help dry AMD – but they only represent an early phase in treatment development. These studies may throw up promising results that are subsequently disproven using bigger, better-designed studies.

While it's encouraging when these types of study show benefits, there are no guarantees the benefits will be confirmed when tested more rigorously.

What did the research involve?

The study recruited 26 patients over the age of 50 with a dry AMD diagnosis, with many large soft deposits of drusen causing disruption to cell layers of the back of the eye.

They were all given a high-dose (80mg) of a statin called atorvastatin every day for 12 months, and knew what they were taking and why.

Each had comprehensive eye exams at the start of the trial and every three months after to monitor changes, including the size and number of drusen deposits. Clarity of vision was measured every six months by reading letters at ever-decreasing sizes through corrective lenses, similar to the classic Snellen eye test sometimes done at opticians.

As dry AMD is a progressive disease, they were looking for signs the disease was being slowed, halted or reversed – any of these would be an improvement over current treatment options.

The study also reported the experimental case of a 63-year-old man with dry AMD who took progressively higher doses of atorvastatin than the target 80mg per day in response to deteriorating visual clarity.

What were the basic results?

Of the 26 participants, 23 made it to at least the end of the first 12 months: 10 from Europe, 13 from the US. Three exited the study early: one because of cramps, one because of muscle aches, and one because they felt the drug was inducing hair loss.

Daily high-dose atorvastatin for a year resulted in fewer drusen deposits in 10 of the 23 participants (43%), and near-complete disappearance in eight people.

Ten of those taking atorvastatin improved their visual clarity, by an average of 3.3 letters on a letter chart. This compared to an average loss of 2.3 letters over the same period for those in whom it didn't work. These differences however, were not statistically significant, meaning it may be a chance finding.

The case of the 63-year-old man was much more dramatic. After six months on 80mg daily atorvastatin, his visual clarity improved by 12 letters and the drusen deposits had completely disappeared, leaving him with 20/20 vision.

How did the researchers interpret the results?

The researchers concluded that: "High-dose statins may result in resolution of drusenoid pigment epithelial detachments (PEDs) [drusen deposits] and improvement in visual acuity [clarity of vision]" adding, "Confirmation from larger studies is warranted".


The difference between the dramatic improvement seen in the case study of the 63-year-old man and the comparatively modest, or lack of, effect seen in the 23 taking part in the trial shows the limitations of studying small numbers of people, and the current uncertainly about the effects of this treatment.

There is large variability in small groups, which doesn't tell us whether the treatment will help most people. The way to solve this is to study lots more people. This helps to smooth out the natural variability in people's responses to the same treatment and can highlight groups more or less likely to benefit. These groups can be studied further to figure out why the variation exists and potentially discover other ways to help more people benefit.

Other limitations include that this study was very small, treatment was not randomised, there was no treatment concealment (blinding), there was no control group, and the visual improvements reported between treatment responders and non-responders might have been due to chance.

The study also focused on people with dry AMD with a high number of large soft drusen deposits, which is a sub-group people with dry AMD. These are all limitations, but understandable ones given the very early stage of this research.

As AMD is so variable, the researchers point out that it's unlikely that statins would be effective for everyone with the condition.

The good news is that there were some signs statins improved vision in dry AMD. However, there was a lot of variation and only 43% of those in the trial experienced an improvement in their sight.

Larger studies are needed to look into statins as a possible treatment for AMD. It's not currently advisable to take statins for dry AMD, as there isn't enough evidence.

Links To The Headlines

Statins could be miracle cure for blindness: Pills could destroy fats that clog the eye. Daily Express, February 5 2016

Could statins help restore vision? Drugs found to clear away deposits that cause blindness in the elderly. Mail Online, February 4 2016

Statin drug could restore eyesight to patients with common form of blindness, say scientists. Daily Mirror, February 4 2016

Statins could reverse most common form of blindness. The Telegraph, February 4 2016

Links To Science

Miller JW, Vavvas DG, Daniels AB, et al. Regression of some high-risk features of age-related macular degeneration (AMD) in patients receiving intensive statin treatment. EBioMedicine. Published online February 4 2016

Categories: NHS Choices

Smoking bans linked to fewer heart attacks and strokes

Thu, 04/02/2016 - 00:00

The ban on smoking indoors in public places "has helped save the lives of passive smokers," says the Daily Mail.

The headline refers to a review of the effects of smoking bans in 21 countries, including England and Scotland. This found fewer admissions to hospitals for heart attacks and strokes following smoking bans. However, the bans didn't appear to encourage more people to stop smoking.

Some studies included in the review found a bigger reduction in heart attacks and strokes among non-smokers – who are no longer exposed to smoke in public places – than smokers, who are still exposed to their own smoke.

The difficulty with research into smoking bans is that you can't carry out the "gold standard" of research: a randomised controlled trial. Instead, we have to rely on observational evidence – for example, looking at trends in hospital admissions for heart attacks before and after a ban is introduced.

It's hard to prove that smoking bans have led to lower hospital admissions, rather than other things, such as putting tobacco prices up. But this research suggests they have, particularly for non-smokers.

Where did the story come from?

The study was carried out by researchers from the Cochrane Tobacco Addiction Group, which is part of the Cochrane Collaboration of international healthcare researchers. It was funded by the Health Research Board Ireland and University College Dublin. The study was published in the peer-reviewed Cochrane Database of Systematic Reviews on an open-access basis, so it is free to read online.

The Sun, Mail Online and The Daily Telegraph focused on results from the smoking ban in England, which was introduced in 2007. While they were reported accurately, these results were published in the British Medical Journal (BMJ) in 2013, so are not particularly new. The Guardian gave a good overview of the research, including links to the original studies.

What kind of research was this?

This was a systematic review of all the studies previously published on the effects of smoking bans on health. Systematic reviews are the best way to get a balanced picture of all the evidence on a topic. However, they are only as good as the studies they include.

In this case, there were no randomised controlled trials, so the researchers had to rely on observational studies of varying quality.

What did the research involve?

This research was an update of a previous systematic review of the evidence around smoking bans, published in 2010. Since then, more countries have introduced smoking bans and more studies have been published.

Researchers searched databases of published research, looking for all relevant studies that met their criteria. They then examined all the studies to record their methodology, results and assess the study for risk of bias.

Usually, Cochrane reviews carry out a meta-analysis, where they pool the data to give overall results from all the studies. Because of the different types of research they found, they were unable to do this for this review. Instead, they grouped together studies looking at the same health outcomes, then summarised the results for each group.

What were the basic results?

Researchers found 77 studies and looked at the effects of a smoking ban on:

  • cardiovascular health (mainly heart attacks and strokes)
  • respiratory health (mainly asthma and chronic obstructive pulmonary disease, or COPD)
  • the health of newborn babies
  • numbers of deaths from smoking-related diseases
  • numbers of people who smoked, plus quit rates and tobacco consumption

They found "persuasive" evidence from 33 out of 43 studies that fewer people were admitted to hospitals with heart attacks and unstable angina, and evidence from five out of six studies that fewer people were admitted with stroke. Some studies found that non-smokers benefited from a bigger reduction in the incidence of heart attack and stroke.

The review also found national rates of smoking-related diseases (including heart disease) went down after smoking bans were introduced, and continued to fall. Eight out of 11 studies showed a reduction in deaths from smoking-related diseases.

The picture was mixed for respiratory health, with conflicting results from the 21 studies reviewed; some found a reduction in COPD or asthma admissions, but others did not.

The researchers found pregnant women were less likely to smoke after bans had been introduced, and some studies found fewer babies were born prematurely or with low birth weight. However, they say the quality of the evidence was too low and the study results were too conflicting to be sure.

The evidence was also unclear about the effect smoking bans had on how much people smoked, and how many smoked. While some studies showed a dip in smoking and an increase in attempts to quit just before and shortly after a smoking ban was introduced, these reductions didn't last.

As most countries were already showing a trend away from smoking, it's difficult to determine whether the bans played a part. Other factors, such as the price of tobacco and economic outlook in a country, might have affected the results.

How did the researchers interpret the results?

The researchers said the results gave "more robust support" for their previous conclusions that smoking bans were linked to better health outcomes. "There is moderate quality evidence that countries and their populations benefit from enacting national legislative smoking bans with improved health outcomes from reduced exposures to passive smoke, specifically cardiovascular disease," they said.

However, they added that the evidence for fewer deaths from smoking-related diseases was "low quality".


There is no doubt that tobacco smoking harms health and causes a great deal of disease and death. The World Health Organization (WHO) estimates that tobacco is responsible for one in 10 adult deaths worldwide.

The question is whether smoking bans can help reduce the harm caused by tobacco. This summary of research suggests they can, particularly for people who are non-smokers. While it's hard to get good-quality evidence about the effects of smoking bans, comparisons of data from hospitals and national registries before and after a ban is helpful.

However, we can't be sure the effects being measured are solely down to the smoking ban. For example, bans on trans fats in foods in some countries could also have contributed to a drop in heart attacks and stroke. However, it's useful to have information from lots of different countries, all showing similar trends over time.

The evidence around the numbers of people who stop smoking after a smoking ban is disappointing, but the researchers point out that smoking bans are only one way to encourage people to quit.

If the effects of a smoking ban are simply to protect people who don't smoke from the harmful effects of tobacco, that is still a big improvement.

Read more information and support about how to give up smoking

Links To The Headlines

Smoking ban sees 40 per cent cut in heart attacks in UK since 2007 law was introduced. The Telegraph, February 4 2016

Smoking bans reduce harm from passive smoking, study finds. The Guardian, February 4 2016

Heart attack rates have fallen by 42 per cent since the smoking ban in 2007. The Sun, February 4 2016

Ban has helped save the lives of passive smokers: Number of heart disease cases has dropped 'significantly' following introduction of laws. Mail Online, February 4 2016 

Links To Science

Frazer K, Callinan JE, McHugh J et al. Legislative smoking bans for reducing harms from secondhand smoke exposure, smoking prevalence and tobacco consumption. Cochrane Database of Systematic Reviews. Published online February 4 2016.

Categories: NHS Choices

Just one hour of sitting down may increase diabetes risk by a fifth

Wed, 03/02/2016 - 14:28

"Every extra hour sitting down can raise your risk of type 2 diabetes by a fifth," the Daily Mirror reports. The paper reports on a study that used an accelerometer – a device that tracks movement – to look at the effects of sedentary behaviour on type 2 diabetes risk.

Researchers in the Netherlands measured the time that almost 2,500 middle-aged or older people spent sitting or lying down in one week, using an accelerometer. They found that people who had type 2 diabetes spent on average 26 minutes longer sitting or lying down, compared to people without diabetes.

From this, the researchers calculated that each additional hour of being sedentary increased the chances of a person having diabetes by 22%. It made little difference whether people sat for long periods or got up for regular breaks – the important thing was the overall amount of time spent sedentary.

Importantly, the study doesn’t tell us if people’s sedentary behaviour led to them getting diabetes, or whether people became more sedentary after getting diabetes. However, it provides more evidence that spending a lot of time physically inactive is likely to be bad for our health.

It is currently thought that the most effective ways you can reduce your type 2 diabetes risk include eating a healthy dietlosing weight (if you're overweight) and becoming more physically active.


Where did the story come from?

The study was carried out by researchers from Maastricht University and was funded by the European Regional Development Fund, numerous institutions from the Netherlands and by grants from three manufacturers of diabetes medication. The study was published in the peer-reviewed journal Diabetologia on an open-access basis, so it’s free to read online.

Most of the UK media’s reporting was accurate, although not all the reports made it clear the study does not prove that being sedentary causes diabetes. The Daily Telegraph did make this clear, while the Daily Mail said researchers had ruled out the possibility that diabetes made people more sedentary, which is not strictly true.

The Sun described sedentary people as "couch potatoes" who were "lazing around" – ignoring the fact that people who work at computers or drive for a living sit for much of the day.


What kind of research was this?

This is a cross-sectional observational study. Researchers wanted to see if people’s activity levels were linked to whether they had type 2 diabetes, or risk factors for type 2 diabetes. Cross-sectional studies can give useful information suggesting a link between two factors – in this case, activity levels and diabetes. However, as snap-shots of information, they can’t tell us whether one causes the other, because we don’t know which factor happened first.


What did the research involve?

Researchers measured the activity levels of 2,497 people aged 40 to 75, 29% of whom had diabetes, using accelerometers. The devices were worn for eight consecutive days and measured whether they were sitting, standing or lying down, as well as speed of movement.

The researchers tested people’s glucose tolerance (a measure for diabetes) and other health measures, such as cholesterol, blood pressure and weight. After adjusting the figures to take account of known diabetes risks, they looked to see whether people’s time spent sitting or lying down was linked to their risk of having diabetes.

As well as whether people actually had diabetes, the researchers considered whether they had impaired glucose tolerance (a restricted ability to process glucose, which is often a precursor of type 2 diabetes) or metabolic syndrome. This is a collection of warning signs for diabetes, including impaired glucose tolerance, a high waist measurement, high levels of unhealthy fats in the blood and high blood pressure.

With the activity data, researchers looked at overall time spent sedentary (other than night-time sleeping), at how many "sedentary breaks" people had – for example, times when they got up and walked around or stood – and for what duration they remained sedentary at any one time.

They adjusted their figures to take account of the following confounders:

  • age
  • sex
  • education level
  • whether they smoked
  • how much alcohol they drank
  • whether they had walking difficulties
  • their health
  • body mass index (BMI)
  • how much higher-intensity exercise they took

Finally, they calculated the risk of having diabetes or metabolic syndrome for each additional hour spent sedentary.


What were the basic results?

People with normal glucose tolerance spent on average 9.28 hours a day sedentary, compared to 9.38 hours for people with impaired glucose tolerance and 9.71 hours for people with diabetes.This means that people with diabetes spent on average 26 minutes longer each day being sedentary.

This equated, said the researchers, to a 22% increased risk of getting diabetes for each additional hour of time spent sedentary (odds ratio [OR] 1.22, 95% confidence interval [CI] 1.13 to 1.32). The chances of having metabolic syndrome was 39% higher (OR 1.39, 95% CI 1.27 to 1.53).

The numbers of sedentary breaks, and duration of sedentary episodes, made little difference once the researchers had adjusted their figures for confounding factors.


How did the researchers interpret the results?

The researchers said this was the first time anyone had shown a link between sedentary behaviour measured by objective accelerometers, and diabetes risk, in a big group of adults. They say their results have "important implications" for public health, and that "consideration should be given to including strategies to reduce the amount of sedentary time in diabetes prevention programmes".

The researchers said their analyses of the data looking specifically at people with more severe diabetes – those taking insulin – suggest that the severity of illness is not linked to the likelihood of being sedentary, so it is more likely that inactivity causes diabetes.



This study adds to existing evidence which suggests the amount of time we spend physically inactive, either sitting or lying down, could have a poor effect on our health. It does not, however, prove that sitting for long periods causes diabetes.

The study has some strengths, including its size and the fact that activity levels were measured objectively. Activity levels in the Netherlands are likely to be similar to those in the UK, so these findings may also apply to us. However, the cross-sectional design of the study means it cannot show that sedentary behaviour is a cause of diabetes, even when taking account of the researchers’ assertion that their analysis of people with more severe diabetes makes this more likely.

Although the researchers adjusted their figures to take account of many confounding factors, they did not look at some other lifestyle aspects that could be important in developing diabetes, such as what people ate and family history of diabetes.

Study results aside, we already know that exercise and physical activity are good for cardiovascular health, so it’s not surprising that spending much of your day sitting down is likely to be a bad thing.

It can be hard to keep active if you have a job that requires you to spend a lot of time sitting down, such as being a taxi driver or working on a computer. This study gives one more potential reason to make sure you spend as much time as possible being physically active, whether that’s going to the gym, taking a walk, using the stairs instead of the lift, or just dancing around the kitchen while making dinner.

Read more about how you can incorporate a fitness regime into your day-to-day activities

Links To The Headlines

Too much sitting down raises Type 2 diabetes risks by up to a fifth. Daily Mirror, February 2 2016

Harm chair: Diabetes risk soars the longer you laze, researchers warn. The Sun, February 3 2016

Sitting raises diabetes risk - and the gym won't help: Every hour someone spends being inactive can increase chance of developing Type 2 by a fifth. Mail Online, February 3 2016

An extra hour on the sofa could increase diabetes risk by a fifth. The Daily Telegraph, February 2 2016

Links To Science

van der Berg J, Stehouwer CDA, Bosma H, et al. Associations of total amount and patterns of sedentary behaviour with type 2 diabetes and the metabolic syndrome: The Maastricht Study. Diabetologia. Published online February 2 2016

Categories: NHS Choices

Weight loss in middle age: A warning sign of dementia?

Wed, 03/02/2016 - 12:30

"How losing weight in middle age 'could be a sign of dementia'," the Daily Mail reports. A US study suggests there is an association between middle-age weight change and risk of mild cognitive impairment (MCI) – which, in some cases, can be an early sign of dementia.

Symptoms of MCI include short-term memory loss, problems recalling the right word for something and difficulties with depth perception.

Researchers in the US studied almost 2,000 older adults (aged 70 and over) who didn't have dementia, and followed them for an average of 4.4 years to see if they developed symptoms of MCI. Medical records were used to establish height and weight measurements from middle age (40 to 65 years old).

Participants who developed MCI in later life experienced greater weight loss per decade in middle age than those who did not – 2kg weight loss compared with 1.2kg respectively. This effect was seen in the group as a whole and separately for men, but not for women. 

The researchers suggest that weight loss may have been due to what is called the "anorexia of ageing". This is said to be a dysfunction in the production of certain hormones, which then affects dietary intake and metabolism, which could in theory affect risk of MCI and dementia.

There is currently no proven way to prevent MCI or dementia. However, identifying possible markers could help in terms of earlier diagnosis and appropriate care, which could stem brain deterioration and loss of function.


Where did the story come from?

The study was carried out by researchers from the Mayo Clinic and was funded by the National Institutes of Health, the Mayo Foundation for Medical Education and Research, the Robert H. and Clarice Smith and Abigail van Buren Alzheimer’s Disease Research Program, the Clinical and Translational Science Award, and the National Center for Advancing Translational Sciences.

Some of the researchers have worked, or are currently working, for pharmaceutical companies.

The study was published in the peer-reviewed medical journal JAMA Neurology.

This has been reported accurately by the Daily Mail, The Times and The Daily Telegraph, all of which discuss the inherent limitations of the study. The newspapers also provide a number of quotes from the researchers explaining the findings. 


What kind of research was this?

This was a cohort study which aimed to investigate the association between weight change in middle age and risk of MCI in older age. MCI is a prodromal stage (an initial warning sign) before dementia. The researchers report that an estimated 5-15% of people with MCI progress to dementia each year.

The study was prospective in that it recruited a cohort of older adults and then followed them up for cognitive impairment. However, weight change in middle age was collected from medical records through a retrospective study.

Such study designs are good for finding possible links between an exposure and an outcome, which was the aim of this research. However, they cannot prove cause and effect, as various other factors may be involved.


What did the research involve?

Participants were enrolled in the Mayo Clinic Study of Aging. A random sample of residents aged 70 to 89 from a single US county were selected using the medical records linkage system of the Rochester Epidemiology Project. All participants were required to be dementia-free, and must have had at least one follow-up evaluation and data available on maximum weight and height in midlife.

Evaluation of participants was by a nurse or study coordinator using the Clinical Dementia Rating scale and the Functional Activities Questionnaire.

Further cognitive testing was performed using nine tests to assess four domains:

  • memory
  • executive function
  • language
  • spatial awareness

Participants were classified as having MCI, dementia or being cognitively normal (if they fell within the normal range and did not meet MCI or dementia criteria). All diagnoses were made by consensus judgement of the nurse or study coordinator, physician and neuropsychologist.

At baseline, demographic variables were recorded, as well as medical history, depressive symptoms, history of cigarette smoking, and current medications (assessed from medication bottles at each evaluation). They also took blood tests to identify people carrying a particular gene (apolipoprotein E ε4 – aka: APOE*E4) that has been linked to the development of Alzheimer’s disease. This was adjusted for in their analyses.

Midlife weight and height was established through medical records.


What were the basic results?

The researchers included 1,895 cognitively normal participants at baseline (average age 78.5 years, 50% male). Over an average period of 4.4 years, 524 participants developed MCI. Those who developed MCI were more likely to be older, have cardiovascular disease, diabetes, and be carrying the APOE*E4 gene. 

A significant difference in average weight change per decade was found between participants who developed MCI and those who did not – a loss of 2.0kg compared to a loss of 1.2kg respectively.

When examining by gender, men who developed MCI had significantly greater weight loss than men who did not (2.1 kg loss vs. 1.2kg loss). For women, there was not much of a difference.

The researchers calculated that a larger weight decline per decade was associated with a 4% increased risk of MCI (hazard ratio 1.04, 95% confidence interval 1.02 to 1.06). This was after adjusting for the possible confounding effects of sex, education, and the presence of the APOE*E4 genotype. Statistical modelling found a weight loss of 5kg per decade to correspond to a 24% increased risk of MCI.

No link with development of dementia was reported.


How did the researchers interpret the results?

The researchers say their findings suggest that increasing weight loss per decade from midlife to late life is a marker for MCI and may help to identify people at increased risk.



This study has investigated the association between weight change in midlife and the risk of MCI in older age.

The study found that participants who developed MCI in later life experienced a slightly greater weight loss per decade in middle age than those who did not. This effect was seen in the group as a whole and for men, but was not significant for women.

The main thing to note is that the researchers are not trying to blame the weight change itself on the increased risk of MCI, just that it could be a marker. The researchers suggest that weight loss may have been due to what is called the "anorexia of ageing". This is said to be a dysfunction in the production of certain hormones, which then affects dietary intake and energy metabolism, which could in theory affect risk of cognitive impairment and dementia.

However, this theory cannot be proven by this study. The causes of MCI and more serious dementia-related conditions such as Alzheimer’s disease are poorly understood, apart from ageing and possible hereditary factors. This research has taken account of gender, educational status and one gene associated with Alzheimer’s. However, there may be other relevant health and lifestyle factors that are influencing the outcomes seen and have not been accounted for.

Other limitations of the study, which the researchers openly state, are that it is not possible to detect from the records whether the weight loss in middle age was intentional. The study was also conducted in one US region, so may not be generalisable to other populations.

Early symptoms of cognitive impairment or dementia can be mild and progress gradually, which can be difficult to notice. There is currently no proven way to prevent cognitive impairment or dementia. However, identifying possible markers could help in terms of earlier diagnosis and appropriate care, hopefully stemming brain deterioration and loss of function.

If you are worried about memory problems, it's important to talk to your GP sooner rather than later. Read about the benefits of an early dementia diagnosis

Links To The Headlines

How losing weight in middle age 'could be a sign of dementia': People who shed the pounds between their 40s and 70s are more at risk of memory problems. Daily Mail, February 2 2016

Losing weight in middle age could herald dementia. The Daily Telegraph, February 2 2016

Losing weight in middle age could indicate dementia risk. The Times, February 2 2016

Links To Science


Alhurani RE, Vassilaki M, Aakre JA, et al. Decline in Weight and Incident Mild Cognitive Impairment. JAMA Neurology. Published online February 1 2016

Categories: NHS Choices

UK regulators give go-ahead for 'embryo editing'

Tue, 02/02/2016 - 13:28

"UK scientists have been given the go-ahead by the fertility regulator to genetically modify human embryos," BBC News reports.

The UK body that regulates research into embryos – the Human Fertilisation and Embryology Authority (HFEA) – has given a licence to Dr Kathy Niakan for her research on stem cells at The Francis Crick Institute in London.

The licence provides permission for genome editing techniques to be used on donated embryos for up to 14 days.

The UK is the first country in the world to make this type of research legal. It remains illegal to implant modified embryos in women. 

What is genome editing?

Genome editing uses a range of molecular techniques to make changes to the genome – the complete set of DNA – of individual organisms.

Genome editing can:

  • modify genetic information to create new characteristics
  • remove regions from genomes – for example, those that can cause genetic diseases
  • add genes from other organisms to specific locations within a genome

The editing process modifies the actual nucleotides – the "letters" of DNA (A, T, C, G) – of genetic code.

Dr Niakan plans to use a genome-editing technique called CRISPR-Cas 9, which has become increasingly popular as it is powerful, reliable, quick and relatively inexpensive.

CRISPR-Cas9 uses a combination of the Cas9 protein and a strand of RNA to make breaks in strands of DNA. New genetic code can then be placed inside the breaks, which can allow genetic code to be rewritten. 

What type of research has the HFEA licensed?

Dr Niakan wants to investigate how embryos develop in the first few days after conception.

She wants to see what effects certain genome-modifying techniques – effectively turning some genes "on and off" – has on the development of the embryo.

Learning more about the early days of embryonic development may help improve the success rates of fertility treatments like in vitro fertilisation (IVF). It could also lead to new treatments for women who have a history of recurrent miscarriages

Are there any other potential applications for this technique?

The range of possible applications is huge. Genome editing has already been successfully used in the treatment of one-year-old Layla Richards, who developed acute lymphoblastic leukaemia when she was five months old.

Layla failed to respond to conventional treatment, so staff at Great Ormond Street Hospital asked permission to try a more radical approach, which her parents were happy to give.

In Layla's case, proteins known as transcription activator-like effector nucleases (TALENs) were used as a kind of "molecular scissors" to modify the DNA inside a batch of donated T-cells (an immune cell).

The T-cells were modified to seek out and destroy the abnormal leukaemia cells, while also becoming resistant to the chemotherapy drugs Layla was taking. Layla responded well to the treatment and is now back home with her family.

Other potential applications involve editing embryos conceived by people known to be carriers of genetic mutations that can lead to conditions such as cystic fibrosis and sickle cell anaemia.

It could be possible to remove these mutations from an affected embryo and then implant the modified embryo in the mother. However, this type of research is currently illegal. 

Have any concerns been raised about HFEA's announcement?

It's fair to say the news has caused controversy in some quarters.

Anne Scanlan, education director of the pro-life charity LIFE, released a statement saying: "We do not know what long-term side effects the tampering with some strands of DNA could have on other strands.

"However, once genetic changes have been made they will be irreversible and handed down to future generations."

And Dr David King, director of the watchdog group Human Genetics Alert, is widely quoted in the media as saying: "This is the first step in a well mapped-out process leading to GM [genetically modified] babies, and a future of consumer eugenics."

Advocates of genome editing have attempted to counter these arguments by making the case that the potential benefits of this technology far outweigh any risk. 

Professor Darren Griffin, professor of genetics at the University of Kent, said: "The ruling by the HFEA is a triumph for common sense.

"While it is certain that the prospect of gene editing in human embryos raised a series of ethical issues and challenges, the problem has been dealt with in a balanced manner. It is clear that the potential benefits of the work proposed far outweigh the foreseen risks."   

Links To The Headlines

Scientists get 'gene editing' go-ahead. BBC News, February 1 2016

British researchers get green light to genetically modify human embryos. The Guardian, February 1 2016

British scientists get the go-ahead to genetically modify embryos to understand why some women suffer repeated miscarriages. Daily Mail, February 1 2016

UK scientists get go-ahead for gene-editing human embryos. The Times, February 2 2016 (subscription required)

Categories: NHS Choices

Young women with high-fibre diet may have lower breast cancer risk

Tue, 02/02/2016 - 10:28

"Teenage girls who get their five-a-day cut breast cancer risk by up to 25 per cent," the Daily Mirror reports. 

A US study suggests teenagers and young women who eat a high-fibre diet based on eating plenty of fruit and vegetables have a reduced risk of breast cancer in later life.

This large and lengthy study tracked around 90,000 US female nurses over 20 years. It found that women whose dietary habits during adolescence and early adulthood placed them in the top fifth highest average fibre intake group (top quintile) were around 25% less likely to develop breast cancer compared to women in the bottom quintile.

This raises the suggestion that young women might be able to significantly lower their risk of breast cancer simply by eating more high-fibre foods, such as fruits and vegetables. 

However, other associated diet and lifestyle factors may be affecting this outcome. Even if the link is with high-fibre food, it could still be down to benefits other than fibre found in fruit and veg.

If the link does exist, it's unclear why fibre could prevent breast cancer. One speculation offered in the study is that fibres may reduce levels of circulating oestrogen, which is known to trigger abnormal breast tissue growth.

These uncertainties aside, the study is in line with recommendations to eat at least five portions of fruit or vegetables a day to reduce your risk of a variety of diseases.


Where did the story come from?

The study was carried out by researchers from Harvard T.H. Chan School of Public Health and was funded by the US National Institutes of Health and a grant from the Breast Cancer Research Foundation. One of the authors was supported by the Japan Pharmaceutical Manufacturers Association.

The study was published in the peer-reviewed medical journal Paediatrics.

For the most part, the UK media reported the story accurately, with most highlighting how fruit and vegetables could reduce breast cancer risk by one quarter in their headlines. This figure relates specifically to the breast cancer risk reduction of eating fibre in adolescence and early adult life, comparing the highest fifth of people consuming fibre with the lowest fifth. This is among the largest risk reductions reported; other risk reductions were smaller.


What kind of research was this?

This cohort study investigated whether women eating more fibre might be less likely to develop premenopausal breast cancer later in life.

The research write-up says that previous studies of fibre intake and breast cancer have almost all been non-significant – that is, they were not statistically significant and may be due to chance. However, none of them examined diet during adolescence or early adulthood – a period when the research team say breast cancer risk factors appear to be particularly important.

A cohort study measures changes over time and can highlight associations – for example, between eating lots of fibre in early life and developing breast cancer at a later age. The downsides of cohort studies are that they cannot prove cause and effect, as they involve no randomisation or blinding. People live their lives as they choose, and researchers measure and observe how this relates to the development of different conditions and diseases. 

This means that other factors, such as other elements of a person’s diet and lifestyle, can influence the specific link of interest (called confounding). Researchers can take steps to lessen this risk, such as adjusting for confounders in the analysis, but it is difficult to eliminate the risk entirely.


What did the research involve?

This study analysed data from a US cohort set up in 1976 to investigate women’s health, called the Nurses' Health Study II.

The researchers used dietary information collected from 90,534 premenopausal women via a questionnaire starting in 1991, and documented 2,833 cases of invasive breast cancer in the 20 years after. In 1998, about half of these women (44,263) also completed a questionnaire about their diet during high school (age 14 to 18) with linked data to 1,118 subsequent cases of breast cancer.

Participants were divided into quintiles (fifths) according to their dietary fibre intake and followed up with further questionnaires about their lifestyle and disease history every two years.

The analysis looked at the link between total fibre, soluble fibre and insoluble fibre consumption in adolescence and early adult life, and development of breast cancer.

The stats were adjusted for a large number of potential confounders collected through questionnaires every two years throughout the study, including:

  • age
  • race
  • family history of breast cancer (invasive or benign)
  • smoking habits
  • height
  • body mass index (BMI) at age 18
  • weight change since age 18
  • age at first period
  • how many children women had and their age at first birth
  • oral contraceptive use
  • alcohol intake
  • energy intake
  • menopausal status


What were the basic results?

Among all women, total dietary fibre intake in early adulthood was associated with significantly lower breast cancer risk – around 19% lower (relative risk [RR] for highest versus lowest quintile 0.81; 95% confidence interval [CI] 0.72-0.91).

Higher intakes of soluble fibre (RR for highest versus lowest quintile 0.86; 95% CI 0.77-0.97) and insoluble fibre (RR for highest versus lowest quintile 0.80; 95% CI 0.71-0.90) were each associated with lower breast cancer risk.

Total dietary fibre intake in adolescence was linked with lower breast cancer risk (RR for highest versus lowest quintile 0.84; 95% CI 0.70-1.01) and was borderline statistically significant, meaning it could be due to chance.

For average fibre intake during adolescence and early adult life, the RR comparing highest with lowest quintiles was 0.75 (95% CI 0.62-0.91). This is equivalent to a 25% RR reduction and is the main figure making the headlines.


How did the researchers interpret the results?

The researchers say their findings: "support the hypothesis that higher fiber [sic] intakes reduce BC risk and suggest that intake during adolescence and early adulthood may be particularly important."



This large and long-term cohort study showed that women with the top fifth highest average fibre intake during adolescence and early adulthood were around 25% less likely to develop premenopausal breast cancer decades later than those in the bottom fifth.

This raises the suggestion that young women might be able to significantly lower their risk of breast cancer – the most common cancer in the UK – simply through eating more high-fibre foods such as fruits and vegetables.

However, it’s worth noting a few points before accepting these promising results at face value.

Total dietary fibre intake in adolescence alone was linked with a 16% lower breast cancer risk, but this was borderline statistically significant (p=0.04) meaning there is a 1 in 25 probability it is a chance result. The usual cut-off for saying something is statistically significant is where there is less than a 1 in 20 (p<0.05) probability it is due to chance, so it’s around the threshold.

Given that previous studies of fibre intake and breast cancer have almost all been non-significant, this should raise healthy scepticism on attributing too much importance to the adolescent element of diet.

The more reliable result came when fibre intake from adolescents and early adults were combined. This lead to a 25% reduction.  

The study isn’t conclusive in saying that fibre is protective for breast cancer, although it shows a link in a large number of women. For example, women with higher fibre intake in adolescence showed signs of living healthier lifestyles generally: they were less likely to smoke, more likely to drink less alcohol, and have lower BMIs in adulthood. Although adjusted for in the analysis, these and a wide range of lifestyle factors have had a residual influence on the results. 

The research team also noted that many foods high in fibre also contain many other biologically active ingredients (like flavonoids) so they couldn't rule out the possibility these were driving the health benefits, instead of, or alongside, fibre. 

The study also had a number of limitations that affect the accuracy of its measurements – for example, the fact that women reported their adolescent diet when they were middle aged (33 to 52). It is unlikely they would accurately recall their diets from 20 or so years ago. However, these inaccuracies would make it less likely to find a link, not more.

A 2010 World Cancer Research Fund report, that looked systematically at all evidence related to diet and cancer, said the evidence on fibre was limited, so no conclusions could be drawn. This report is due an update in 2016, which may include the results of this study.

Irrespective of whether fibre on its own, or foods that contain fibre in general, protect against breast cancer, the study is broadly in line with robust evidence suggesting you should consume at least five portions of fruit or vegetables a day. This can reduce your risk of developing a range of chronic diseases, such as heart disease, stroketype 2 diabetes and obesity.

Most people in the UK don’t eat the recommended minimum of five portions of fruit and vegetables a day, so chances are you will benefit from eating more and a larger variety. Read more about how to get your five a day and how to increase the amount of fibre in your diet.

Links To The Headlines

Teenage girls who get their five-a-day cut breast cancer risk by up to 25 per cent. Daily Mirror, February 1 2016

Fruit and veg 'could reduce breast cancer risk by one quarter'. The Daily Telegraph, February 1 2016

Girls told to eat fruit to beat breast cancer: Fibre from five portions can reduce risk by a quarter. Mail Online, February 1 2016

Links To Science

Farvid MS, Eliassen AH, Cho E, et al. Dietary Fiber Intake in Young Adults and Breast Cancer Risk. Pediatrics. Published online February 1 2016

Categories: NHS Choices

Proton beam therapy 'effective' and 'causes fewer side effects'

Mon, 01/02/2016 - 13:00

"Proton beam cancer therapy 'effective with fewer side effects'," BBC News reports. A US study found the technique caused fewer side effects than conventional radiotherapy.

Proton beam therapy hit the headlines in 2014 due to the Ashya King case – with his parents removing him from hospital without the knowledge of staff to receive this treatment abroad. The technique is an alternative to standard radiotherapy. In this study, it was used to treat a malignant brain tumour called medulloblastoma in 59 children.

Medulloblastomas can be cured with a combination of surgery, chemotherapy and radiotherapy. However, standard "photon" radiotherapy is associated with a risk of long-term complications for the child, including hearing problems and cognitive (brain function) impairment.

Photon beam therapy uses beams of protons (sub-atomic particles) to destroy cancerous cells. Unlike conventional radiotherapy, the beam of protons stops once it "hits" the cancerous cells. This results in much less damage to surrounding tissue.

In this study, 16% of the children had serious hearing loss five years after proton beam therapy. This compares favourably with standard radiotherapy, where about 25% have hearing loss. Cognitive impairment was also slightly less – 1.5 intelligence points (IQ) lost per year, compared with 1.9 in studies of standard radiotherapy. Overall survival was reported to be similar to standard radiotherapy. The main limitation is that this was not a randomised controlled trial directly comparing the two forms of radiotherapy – the researchers said this would be unethical.

The results seem promising and the researchers hope their study will pave the way for other studies examining safety and survival outcomes of proton beam radiotherapy in other cancers.


Where did the story come from?

The study was carried out by researchers from Massachusetts General Hospital, Brigham and Women’s Hospital in Boston, and Winship Cancer Institute of Emory University in Atlanta, US. The study was funded by the US National Cancer Institute and Massachusetts General Hospital, and published in the peer-reviewed medical journal The Lancet Oncology.

The partner of the lead author of the study is reported as having stock options in ProCare, a private medical company that provides proton beam therapy.

The UK media's reporting of the study was accurate and, as would be expected, referenced the Ashya King case, which was one of the bigger news stories of 2014.


What kind of research was this?

This was a prospective phase II trial aiming to look at the side effects and survival outcomes of using proton radiotherapy to treat children and young people (aged 3 to 21 years) with medulloblastoma.

Medulloblastoma is a type of brain tumour that starts in the cerebellum – an area found at the base of the brain. It is the most common malignant (cancerous) brain tumour in children. Although it can be cured with a combination of surgery, radiotherapy and chemotherapy, the treatment often leads to long-term complications, such as cognitive and hearing impairment, hormonal problems and risk of other cancers. The researchers say that survivors often have a poorer quality of life than their peers, with complications being greatest for the youngest children.

Proton beam therapy (also known as proton radiotherapy) seems promising in being able to be given at a lower and more targeted dose than standard (photon) radiotherapy, and is increasingly used to minimise side effects of treatment.

A phase II trial primarily aims to see whether a possible new treatment is safe, and also start to get an idea of whether it might be effective and at what doses. This phase II trial was non-randomised and open label (unblinded) – meaning that all people were receiving the same treatment and knew what treatment they were receiving. 

Ideally, if the results of phase II trials are promising, they then progress into larger phase III randomised controlled trials which examine effectiveness and safety in a larger number of people with the condition, compared to inactive placebo or other treatments usually used for the condition. However, the researchers say that in this case, randomising children to different forms of radiotherapy would be unethical.

Despite this being a non-comparative trial, the fact that it was set up prospectively to monitor the effects of this treatment means the data is more likely to be reliable than studies where researchers just look back at people's routine medical notes to see what happened to them.


What did the research involve?

The study recruited children and young people (aged 3 to 21 years) with medulloblastoma, all of whom initially received surgery to remove the tumour. Further diagnosis and staging was then based on laboratory analysis of the tumour and imaging results. Of the 59 participants included, 39 were classified as having standard-risk disease (according to Children's Oncology Group criteria), six with intermediate-risk disease, and 14 with high-risk disease. Their average age was 6.6 years. 

Within 35 days of surgery, all participants received proton radiotherapy delivered to the brain and spinal cord. This was given at a total dose of 18-36 Gy radiobiological equivalents (GyRBE) delivered at 1.8 GyRBE per fraction followed by a boost dose (GyRBE is a measure of the amount of radiation delivered to an area of human tissue). All trial participants received the proton radiotherapy at an average (median) dose of 23.4 GyRBE and a boost dose of 54.0 GyRBE.

All participants also received chemotherapy, which could be given before, during or after radiotherapy.

The average follow-up of participants was seven years. The main (primary) outcome examined was grade 3 or 4 hearing loss at three years after radiotherapy. This level of hearing loss is serious and would mean the child would need treatment such as hearing aids in at least one ear, or cochlear implants, as well as speech-language related services.

The researchers also looked for cognitive (brain function) impairment (assessed at 1, 3, 5 and 7-8 years), and hormonal effects, which were assessed by annual measurements of height, weight and blood hormone levels. They also looked at the proportion of children surviving without their disease progressing (progression-free survival) at three years, and overall survival.


What were the basic results?

Overall, hearing in participants was significantly poorer at follow-up than it had been before treatment. Of 45 children with complete hearing assessments available at three years, 12% had grade 3-4 hearing loss. By five years, grade 3-4 hearing loss had risen to 16%. Four children experienced this hearing loss in both ears, and three in one ear (one of the latter group had improved hearing later on).

Looking at cognitive impairment, IQ decreased by an average of 1.5 points (95% confidence interval [CI] 0.9 to 2.1) per year five years after treatment. The main areas of impairment were information processing speed and verbal comprehension. Just over half of children (55%) had hormonal problems five years after treatment, with low levels of growth hormone being most common. There was no toxicity reported for the heart, lungs or gastrointestinal system. 

Looking at effectiveness, 83% of children were alive and their disease had not progressed at three years, and 80% at five years. Overall, at five-year follow up, 83% of children were alive.


How did the researchers interpret the results?

The researchers conclude: "Proton radiotherapy resulted in acceptable toxicity and had similar survival outcomes to those noted with conventional radiotherapy, suggesting that the use of the treatment may be an alternative to photon-based treatments."



This phase II study looked at the long-term side effects of using proton radiotherapy as part of the treatment of children with medulloblastoma. The treatment was used alongside standard surgical removal and chemotherapy. The current study is reported to be the longest prospective follow-up study available on this treatment for medulloblastoma.

Overall, 12% of the study's participants had severe hearing loss three years after proton radiotherapy, and 16% at five years. This was reported by the authors to be less than the equivalent 23 Gy dose of standard (photon) radiotherapy, which was said to cause hearing loss in about a quarter (25%) of those receiving it. However, as the researchers say, these comparisons are not completely reliable because of the different doses used.

Cognitive impairment was also slightly less than has been observed with standard radiotherapy – 1.5 IQ points in this study, and 1.9 with photon radiotherapy in other studies. Again, the researchers caution over the differences in radiation doses used and population treated. 

Progression-free and overall survival rates in this study were reported to be much the same as those using standard radiotherapy. There was also a lack of reported toxic effects to the heart, lungs or digestive system.       

Overall, the results seem positive. The difficulty is that this is a non-comparative trial. All children received proton radiotherapy. There was no randomised comparison group with similar characteristics in terms of tumour type, stage, surgery and chemotherapy treatment who instead received standard radiotherapy, to directly compare complications and survival outcomes. Ideally, a large number of children randomised to the same dose schedule of the two forms of radiotherapy would be needed to give the best comparative information on effectiveness and safety.

However, the researchers say: "Although a randomised trial is the best way to obtain a proper comparison cohort, both clinical leaders in the UK and the US deem randomised trials of proton and photon radiotherapy in children to be both unethical and not feasible". This means that such trials are unlikely to be carried out, and this type of prospective non-comparative study is likely to be the best evidence available.

The researchers suggest their findings of an acceptable toxicity profile and similar survival outcomes of proton compared to standard radiotherapy mean, "This study could serve as a template for other outcomes-based studies in different populations to better define the role of proton radiotherapy for the treatment of other cancers."  

Links To The Headlines

Proton beam cancer therapy 'effective with fewer side effects'. BBC News, January 30 2016

Proton beam therapy has fewer harsh side effects, according to child cancer study. The Guardian, January 30 2016

So Ashya's parents were RIGHT: Proton beam cancer therapy that forced family to go on the run to Spain because they couldn't get it on the NHS is as good as chemotherapy - and has fewer side effects. Mail Online, January 30 2016

Proton beam therapy: Cancer treatment that 'cured' Ashya King is effective and has fewer side effects, study finds. The Independent, January 30 2016

Ashya King proton beam cancer therapy 'causes fewer side effects'. The Daily Telegraph, January 30 2016

Ashya King's mother: Proton beam therapy saved my cancer child's life. Daily Express, January 30 2016

Links To Science

Yock TI, Yeap BY, Ebb DH, et al. Long-term toxic effects of proton radiotherapy for paediatric medulloblastoma: a phase 2 single-arm study. The Lancet Oncology. Published online January 29 2016

Categories: NHS Choices

High-flavonoid foods, like berries and apples, 'prevent weight gain'

Fri, 29/01/2016 - 11:00

"Get fruity to get fit: Eat more berries to beat a big belly," The Sun reports. The advice is based on the findings of a major new study looking at the effects of foods rich in the compound flavonoid, such as berries and apples, on body weight.

The researchers tracked around quarter of a million people over 24 years.

Results suggest that eating more flavonoids – specifically anthocyanins (coming mainly from blueberries and strawberries), flavonoid polymers (from tea and apples), and flavonols (from tea and onions) – was linked to less weight gain.

Every extra 10 milligrams (mg) of anthocyanins, 138mg of flavonoid polymers, and 7mg of flavanols per day, was linked to 70-100g less weight gained over four-year intervals. While this may not seem a lot, it adds up over a number of years.

An inherent limitation of this type of study design is that it cannot prove cause and effect – it can only highlight associations.

It would be unwise to take this study as advice to only eat berries or apples, as a balanced diet containing a wide variety of fruits and vegetables remains important for overall health.  Nonetheless, the study is broadly in line with more robust evidence suggesting you should consume at least five portions of fruit or vegetables a day to reduce your risk of a variety of diseases.

Age-related weight gain – the dreaded "middle-aged spread" – is common, but not inevitable.

Find out how to start losing weight


Where did the story come from?

The study was carried out by researchers from the Chan School of Public Health, Beth Israel Deaconess Medical Center, Brigham and Women’s Hospital, and Harvard Medical School, all based in Boston (US), and the Norwich Medical School, University of East Anglia (UK). It was funded by the US National Institutes of Health, and the Biotechnology and Biological Sciences Research Council (BBSRC).

Two of the authors reported that they had received grants from the US Highbush Blueberry Council. These grants were unrelated to this study.

The study was published in the peer-reviewed British Medical Journal (BMJ) on an open-access basis, so you can read it for free online.

The UK media generally reported the facts of the study accurately, but most didn’t highlight the limitations of the study design, which the researchers themselves went out of their way to do.

Importantly, the study made no guarantees that if you eat or drink more flavonoids, you’d lose weight or be more likely to be a healthy weight. People eating flavonoids might have diets that are healthier in many ways, such as being high in fibre, which could explain why they are better able to maintain a healthy weight over the long term than people reporting lower flavonoid intakes. All, some or none of the weight benefits may relate directly to flavonoids.

The Daily Mirror sensibly pointed out that although flavonoids are found in various types of chocolate and wine, the calories may counter any positive weight loss effect.


What kind of research was this?

This research combined results from three cohort studies looking at whether dietary intake of specific flavonoid subclasses (including flavonols, flavones, flavanones, flavan-3-ols, anthocyanins, and flavonoid polymers) was associated with weight change over time.

The study team describe how previous studies show that those who eat more fruit and veg are more likely to maintain a healthy weight, which is unsurprising. What is less clear is the specific mechanism by which the fruit and vegetables lead to a healthy weight, or prevent weight gain.

This study looked specifically at the flavonoids, to see whether they were the crucial weight-maintaining ingredients. 

Readers should be aware that these types of studies can find associations between consumption of certain food ingredients (like flavonoids) with weight gain or other health benefits. However, they cannot prove that by increasing your consumption of flavonoids you will put on less weight than if you didn’t. A study where you randomly assign people a diet high in flavonoids for a long period of time would be needed to test this, and may not be the most practical to implement. Most people don’t follow diets given to them for long periods. 


What did the research involve?

The study analysed diet and weight change information on 124,086 adult health professionals over 20 to 24 years from three cohort studies in the US: the Health Professionals Follow-up Study (HPFS), Nurses’ Health Study (NHS), and Nurses’ Health Study II (NHS II).

Self-reported change in weight was collected every two years via a questionnaire and was converted into a weight change measure spanning four-year intervals.

All participants self-reported their diet every four years using a validated, food frequency questionnaire. Foods were looked up on a US Department of Agriculture database to estimate their flavonoids content.

Information on other lifestyle habits were collected every four years via the same questionnaire. This was then incorporated into the analysis to minimise their effects, in an effort to isolate the effect of flavonoids. This adjustment of the analysis for confounders included the following variables:

  • age
  • body mass index (BMI)
  • change in smoking status
  • physical activity level
  • hours of sitting or watching TV
  • hours of sleep over the same time period

They also took into account changes in intake of the following foods/nutrients:

  • fried potatoes
  • juice
  • whole grains
  • refined grains
  • fried foods
  • nuts
  • whole-fat dairy
  • low-fat dairy
  • sugar-sweetened drinks
  • diet drinks
  • sweets
  • processed meats
  • non-processed meats
  • trans fat
  • alcohol
  • seafood
  • caffeine

Citrus juices were a main source of both flavone and flavanone intake in the study, so the researchers used non-citrus juice rather than all-fruit juice as a covariate for analyses of these two flavonoid subclasses. In additional models, they further adjusted for change in total fibre intake (g/day).

People with chronic disease at study start were excluded, due to the risk of their disease causing weight loss – messing up any link with flavonoids. This included some very common conditions like being obese (with a BMI of 30 or over) or having diabetes. This means the study group are a particularly healthy sub-group of the US general population, which is something we should bear in mind when interpreting the results.

The main analysis looked for links between four-year change in weight and change in intake of flavonoid subclasses over the same period, having adjusted for the long list of likely confounders.


What were the basic results?

Average age over the three cohorts was 36 to 49 (range 27 to 65) and over each four-year period, people gained an average of 1-2kg.

Consumption of most flavonoid subclasses (with the exception of flavones and flavanones) was associated with less weight gain among men and women aged 27-65 followed for up to 24 years.

The greatest magnitude of association was observed for anthocyanins (coming mainly from blueberries and strawberries), flavonoid polymers (from tea and apples), and flavonols (from tea and onions). Each set increase in anthocyanins (10mg), flavonoid polymers (138mg), and flavonols (7mg) was linked to 70-100g less weight gained over four-year intervals.

These associations remained statistically significant for anthocyanins and flavonoid polymers (including proanthocyanidins alone) after further adjustment for fibre intake, which was inversely associated with weight change in all three cohorts. This suggested that high anthocyanin and flavonoid polymer food sources may be associated with less weight gain through mechanisms other than fibre content.

The study repeated the analysis in those who were obese in the study and found the same links. These people had become obese while taking part in the study; obese people were excluded at the study outset.


How did the researchers interpret the results?

The researchers concluded that: "Higher intake of foods rich in flavonols, flavan-3-ols, anthocyanins, and flavonoid polymers may contribute to weight maintenance in adulthood and may help to refine dietary recommendations for the prevention of obesity and its potential consequences."

The research team describe the magnitude of the effect as "small" but pointed out then even small decreases in weight gain may have an important public health impact. For example, they cite two studies they say suggest that "losing just 11-22lbs (5.0-10kg) is associated with a decrease in blood pressure". Bearing in mind that the maximum difference was 100g less weight gained per four years, it would take around 200 years to achieve this. 



This study found that people who ate more flavonoids, specifically anthocyanins (coming mainly from blueberries and strawberries), flavonoid polymers (from tea and apples), and flavonols (from tea and onions), gained less weight than those consuming less over a 24-year period. Every extra 10mg of anthocyanins, 138mg of flavonoid polymers, and 7mg of flavonols was linked to 70-100g less weight gained over four-year intervals. This isn’t a lot, but adds up over the years.

Readers should be aware that cohort studies like this can find associations between consumption of certain food ingredients (like flavonoids) with weight gain or other health benefits, but they cannot prove that by increasing your consumption of flavonoids you will put on less weight. A study where you randomly assign people a diet high in flavonoids for a long period of time would be needed to test this, and may not be the most practical to implement.

However, the results are consistent with general public health advice to eat lots of fruit and vegetables. Most people in the UK don’t eat the recommended minimum of five portions of fruit or vegetables per day, so you may benefit from eating more and a larger variety.

The study was large and long term – both big strengths, thereby increasing the reliability of the findings.

However, no study is perfect and the study authors pointed out the major limitations of their work.

Firstly, the accuracy of estimates of flavonoid content can be affected by ripeness, storage conditions, food processing, and season. This measurement error would make it less likely to find the association the study did and may underestimate the effect of flavonoids on weight gain.

The results could again underestimate true associations if people who gained weight at the beginning of a four-year period modified their diet in response, eating more fruits and vegetables (flavonoids) to lose weight (reverse causality). On the other hand, the results could overestimate true associations if people who gained weight stopped eating fruits and vegetables.

Individuals who eat more flavonoid-rich foods like fruit and vegetables may have other lifestyle or dietary habits that lead them to put on less weight. The study made many practical efforts to limit this effect, such as controlling for fibre, smoking and many other foods, but may not have completely eliminated the meddling influence of other compounds on any potential flavonoid weight link.

Hence, we must be very careful about recommending high-flavonoid foods as being beneficial to health, although consuming at least five portions of fruit or vegetables a day has significant health benefits.

A healthy diet, while beneficial, may not be enough to prevent weight gain or help you lose previously gained weight. Regular exercise is also needed.

Read more about diet and exercise and how the NHS Choices weight loss guide uses both to help you lose weight.  

Links To The Headlines

Get fruity to get fit: Eat more berries to beat a big belly. The Sun, January 28 2016

Eating berries and drinking tea crucial in maintaining a healthy weight into old age. The Mirror, January 28 2016

Fruit and vegetables high in flavonoids may help prevent weight gain. The Daily Telegraph, January 28 2016

Natural compound in fruit and veg could help prevent weight gain – study. The Guardian, January 27 2016

How an apple a day helps keep the pounds away: Fruit and veg high in plant compounds can reduce amount of energy absorbed from foods. Mail Online, January 28 2016

Links To Science

Bertoia ML, Rimm EB, Mukamal KJ, et al. Dietary flavonoid intake and weight maintenance: three prospective cohorts of 124 086 US men and women followed for up to 24 years. BMJ. Published online January 28 2016

Categories: NHS Choices

Antidepressants linked to suicide and aggression in teens

Thu, 28/01/2016 - 11:00

"Antidepressant use doubles the risk of suicide in under 18s and the risks to adults may have been seriously underestimated," The Daily Telegraph reports.

A review of clinical study reports compiled by drug companies also suggests that risks may have been under-reported. Clinical study reports usually have more detail than the summaries of published trial results.

Researchers analysed 70 studies which looked at five antidepressants.

They looked specifically at the reports of deaths, suicides, suicidal thinking or suicide attempts, aggression, and a type of extreme restlessness called akathisia.

The results showed that children taking antidepressants had a higher chance of suicidal thoughts or suicide attempts, and of aggression. None of the children in the studied died. Adults in the studies did not have an increased risk of these problems.

The finding that children and young people are more likely to think about or attempt suicide while taking antidepressants is not new, and has been known for more than a decade.

The study authors criticised the small amount of data on harms available, and the way it was presented. They say this makes it difficult to calculate the true chance of harm from antidepressants.

It is a potential concern that harms may have been under-reported by pharmaceutical companies. Only full disclosure of evidence can provide us with an accurate profile of both the risks and benefits of a treatment.

No-one should stop taking an antidepressant suddenly as a result of this study. If you are concerned about the risk of side effects, see your doctor. Stopping antidepressants suddenly can be dangerous. 

Where did the story come from?

The study was carried out by researchers from the Nordic Cochrane Centre and the University of Copenhagen, and was funded by the Laura and John Arnold Foundation. The study was published in the peer-reviewed British Medical Journal (BMJ) on an open-access basis, so it can be read for free online.

The UK’s media reports focused on the potential increased risk of children becoming suicidal, seemingly unaware that this is a long-established risk. The Daily Telegraph blurs the findings, with its headline reporting that "Antidepressants can raise the risk of suicide," without making it clear that this only applies to under-18s.

Most of the headlines failed to make clear that the increase in suicide risk, while statistically significant, was small.

These criticisms aside, the general quality of the reporting was good, with many useful quotes from independent experts.


What kind of research was this?

This was a systematic review and meta-analysis of randomised controlled trials (RCTs) of antidepressants.

This is usually the best type of study for establishing the effects of drugs. However, a systematic review is only as good as the studies that go into it.


What did the research involve?

Researchers looked at detailed information for all RCTs of antidepressants in the classes of selective serotonin reuptake inhibitor (SSRI), including fluoxetine and paroxetine, or selective noradrenaline reuptake inhibitor (SNRI), including venlafaxine.

They included any studies that had information on harms to individual patients (as opposed to just summaries of harms). They worked from clinical study reports, which usually have more detail than the summaries of trial results published. Clinical study reports are submitted to regulatory authorities prior to a drug being granted a license.

The researchers pooled the data from the studies to see how common certain harms were in people who had taken the study drug, compared to people who had taken placebo. They then looked separately at the results for people under and over the age of 18.

Using these results, they calculated the risk of four specific harms from taking the antidepressants studied: death, suicidality (meaning suicidal thoughts, suicide attempts or self-harm), aggression and akathisia (an unpleasant sense of restlessness and agitation, which has been described as "feeling like I wanted to jump out of my skin").


What were the basic results?

Researchers looked at clinical study reports from 70 studies into duloxetine, fluoxetine, paroxetine, sertraline and venlafaxine, covering 18,526 patients.

Overall results

Overall, they found no statistically significant increased risk of death, suicidality or akathisia among people taking the study drugs. They did find an overall increased risk of aggressive behaviour, which was almost doubled in people taking the drugs compared to people taking placebo (odds ratio [OR] 1.93, 95% confidence interval [CI] 1.26 to 2.95). However, this affected a very small number of people, at 5.7 people per 1,000 taking antidepressants, compared to 3.8 per 1,000 people taking placebo.

Results in adults

When they looked at the risks separately for adults, they found no increased risk of any of the outcomes.

Results in children

Looking separately at results for under-18s, they found that children and adolescents did have increased risks of suicidality, at 3 in 100 for those taking antidepressants, compared to 1 in 100 on placebo (OR 2.39, 95% CI 1.31 to 4.33). Similar results occurred for aggression, at just under 4 in 100 for those on antidepressants, compared to 1 in 100 on placebo (OR 2.79, 95% CI 1.62 to 4.81).


How did the researchers interpret the results?

The researchers said that many of the studies did not clearly report harms from treatments, and that some were misclassified or described as something else (for example, "suicidal thoughts" were sometimes classified as "worsening depression"). Because of this, they say, "The true risk for serious harms [from antidepressants] is still uncertain. The low incidence of these rare events and the poor design and reporting of these trials makes it difficult to get accurate effect estimates."

The researchers report that in several instances, deaths were misclassified as happening after the end of the trial, even though they were still within the trial's timespan. They also question whether the side effect of akathisia is under-reported, because in some trials the term did not appear at all, suggesting that it is being classified as something else.

They suggest "minimal use" of antidepressants in children, adolescents and young adults, and that people in these age groups should be offered alternative treatments, such as exercise and psychotherapy.



Perhaps the most troubling aspect of this paper is not the increased risk of suicidal thoughts in young people, as that has been known for many years. What is worrying is the researchers’ conclusion that they are unable to tell the true extent of harms from antidepressants, because of poor data collection and availability.

RCTs are designed to test the effects of treatments with as little bias as possible. However, if the right data on adverse effects is not collected in the trials, or is not made public, we cannot balance the benefits and risks of treatment in a fair and transparent way.

According to the data we do have, it is likely that for many people, the benefits of antidepressant treatment will outweigh the risks. The situation is different among under-18s, as doctors have known since 2004, when warnings against using certain antidepressants in children were issued.

Guidelines on the treatment of depression in children say antidepressants should only be considered for children with moderate to severe depression if psychological (talking) therapy has not helped, and after a specialist review and discussion with the child and their family. In this instance, only fluoxetine is recommended.

It is worth repeating that it can be dangerous to stop taking antidepressants suddenly. Some people get a withdrawal syndrome, which can make depression much worse. If you are worried about taking antidepressants, or feel they are not helping you, make an appointment with your doctor.

If you or anyone you know feels like harming themselves or is considering suicide, you can call The Samaritans on 116 123 any time, in complete confidence. You should also seek medical help immediately.

Links To The Headlines

Antidepressants can raise the risk of suicide, biggest ever review finds. The Daily Telegraph, January 28 2016

'Suicide risk' to teenagers who take antidepressants: Chance of suicidal behaviour or aggression is doubled when taking one of five common drugs. Daily Mail, January 28 2016

Common antidepressant 'could put children at greater risk of suicide'. The Guardian, January 28 2016

Children given antidepressants are twice as likely to become suicidal, claims new study. The Independent, January 28 2016

Links To Science

Sharma T, Guski LS, Freund N, Gøtzsche PC. Suicidality and aggression during antidepressant treatment: systematic review and meta-analyses based on clinical study reports. BMJ. Published online January 27 2016

Categories: NHS Choices

New clues that Alzheimer’s may have been spread during surgery

Wed, 27/01/2016 - 13:30

"Researchers have reported a second case that suggest [sic] Alzheimer's can be transmitted during medical treatments," the Mail Online reports.

Researchers carried out autopsies of seven people who died from Creutzfeld Jakob Disease (CJD) after a procedure called a dural graft, which is often used to repair severe head injuries and treat brain tumours.

This involved taking a section of the dura – the membrane surrounding the brain – from a person who had recently passed away. Unfortunately, in these seven cases, the tissue was contaminated with the CJD prion. Dural grafting is also now done using artificial material, not material derived from human brains.

In five out of the seven cases, researchers also found abnormal proteins associated with Alzheimer's disease. These are called amyloid beta proteins, which have been described as the "seeds" of Alzheimer's.

The question is: could the grafting procedure have introduced amyloid beta protein, as well as prions? And could this have theoretically caused Alzheimer's disease if they had not died of CJD?

The research was carried out after a previous study in 2015 unexpectedly found amyloid protein in brains of some people in the UK who had died of CJD after being infected by injections of contaminated human growth hormone.

Neither study proves that Alzheimer's disease is caused by amyloid beta proteins, or that they can be passed on by surgery.

Some experts have raised the issue that amyloid beta protein are very "sticky" and if they can be passed on, that more stringent sterilisation procedures of surgical instruments may be required.   


Where did the story come from?

The study was carried out by researchers from University Hospital Zurich and Medical University Vienna. It had no specific funding. 

The study was published in the online peer-reviewed journal Swiss Medical Weekly, and is available on an open-access basis, so it is free to read online.

The quality of the reporting in the Mail Online and the Daily Mirror was accurate, balanced, and in the case of the Mail, particularly informative. Unfortunately, these factors were undermined by unnecessarily alarmist headlines.

The Mail's headline, asking: "Can you catch Alzheimer's?" and the Mirror's question: "Is Alzheimer's passed from person to person?" suggest that people might get the disease directly from being in contact with or caring for someone with dementia. This is completely untrue and could cause unnecessary fear and distress.


What kind of research was this?

This was a case-controlled study, involving post-mortem pathological investigations of the brains of patients who had died from CJD caused by brain surgery. CJD related to surgery is known as iatrogenic CJD. Iatrogenic CJD is now extremely rare in the UK, due to a greater understanding of the underlying risks.

Observational studies such as this can compare groups to see whether something is more common in one group than another, but cannot show the reasons.


What did the research involve?

Researchers looked at the brains of seven people who had died of CJD, years after having dural grafting surgery. They tested the brains for the presence of two proteins linked to Alzheimer's disease – amyloid beta protein and tau protein. They compared the results to tests on brains of people who had died of CJD not caused by medical accidents (sporadic CJD).

Each of the seven brains was compared to three brains of people the same age, who had died of sporadic CJD. The researchers also tested a series of 81 cases of sporadic CJD, not matched for age but in a similar age range. They looked for amyloid beta protein in the blood vessels of the brain (cerebral amyloid angiopathy) and as plaques in the brain's grey matter.

The researchers wanted to see whether amyloid beta protein was more common in the brains of people who had got CJD after dural grafting surgery, compared to people who got CJD without having been infected by a medical accident. They looked to see whether people's age, or the length of time since they'd had surgery before dying of CJD, made any difference to the results.


What were the basic results?

Five of the seven (71%) brains of people who'd died of CJD after dural grafting contained amyloid beta proteins. All of these had amyloid proteins, both in blood vessels in the brain and as plaques. 

Among the brains of people the same age, who'd died of sporadic CJD, one had amyloid beta in brain blood vessels (5%) and five had amyloid plaques (24%). Among the big group who'd died of sporadic CJD, 11% had amyloid beta in either blood vessels or plaques in the brain. Statistical analysis showed that amyloid protein was far more common among people with CJD who'd had dural grafts.

The people who'd had dural grafting and also had signs of amyloid beta were aged 28, 33, 47, 52 and 63. They'd had dural grafting more than 20 years before their deaths. The two people who did not show signs of amyloid beta were aged 51 and 59, and had received dural grafts 11 to 12 years earlier. 

None of the brains studied showed signs of tau, the other protein linked to Alzheimer's disease.


How did the researchers interpret the results?

The researchers said: "The presence of amyloid beta pathology in young individuals who present with neither a family history of early-onset dementia or prominent AD-related tau pathology is highly unusual and suggests a causal relationship to the dural grafts."

In other words, they say, it is "plausible" that the amyloid proteins in the brains had not arisen naturally as part of ageing, or because people had genes predisposing them to Alzheimer's disease, but that they had been deposited in the brains during the dural graft surgery.

They say there are other possible explanations – for example, that the head injury or brain tumour which led to the dural graft surgery could also have led to the presence of amyloid beta in the brain. They point out that we don't know whether potential transmission of amyloid beta protein into the brain could actually cause Alzheimer's disease.

However, they call for a "critical re-evaluation" of decontamination procedures for surgical instruments and drugs derived from human tissue, to prevent possible contamination being passed on during medical treatment.



This latest research adds some evidence to the possibility that amyloid beta proteins could have been passed on during certain types of treatment, which introduced substances derived from donor brains or pituitary glands into the body. However, these types of treatment are no longer used.

The theory is far from certain, and other possible causes need to be investigated. Even if the theory was proven, we don't know that having these proteins introduced into the brain in this way would cause Alzheimer's disease. All the evidence showing amyloid protein in the brain after medical treatment has come from studies of the brains of people known to have been infected with prions causing CJD. None of these people actually showed outward signs of Alzheimer's.

There is absolutely no need to worry about "catching" Alzheimer's disease through day-to-day contact with people who have the disease, whether you are a carer or a family member.

There is no reason to think the condition has been passed on through routine surgery or blood transfusions. However, doctors will want to look at how instruments are decontaminated, to ensure that the precautions now taken against passing on prion diseases are also adequate to protect against possible transmission of amyloid beta protein.

Links To The Headlines

Can you CATCH Alzheimer's? Fresh fears emerge amid claims of a second case of transmission from a transplant. Mail Online, January 26 2016

Is Alzheimer's passed from person to person? Fears grow that disease could be transmitted through 'medical accidents'. Daily Mirror, January 26 2016

More evidence emerges for 'transmissible Alzheimer's' theory. Nature, January 26 2016

Links To Science

Frontzek K, Lutz MI, Aguzzi A, et al. Amyloid-β pathology and cerebral amyloid angiopathy are frequent in iatrogenic Creutzfeldt-Jakob disease after dural grafting. Swiss Medical Weekly. Published online January 26 2016

Categories: NHS Choices

'Autistic' monkeys created in controversial study

Tue, 26/01/2016 - 10:30

"Genetically modified (GM) monkeys that develop symptoms of autism have been created to help scientists discover treatments for the condition," The Guardian reports. 

The reports are based on news that Chinese researchers have created monkeys with autistic traits using gene editing techniques.

The monkeys were modified to possess the human gene MECP2. Mutations in this gene or carrying too many copies of the gene in humans has been linked to autistic spectrum disorder (ASD). ASD affects social interaction, communication, interests and behaviour.

The researchers wanted to test whether the genetically modified monkeys would show autism-like behaviours and if they were able to pass this gene on to their offspring. 

The researchers found that the modified monkeys did show certain autism-like behaviours. These included increased frequency of repetitive movement in a circle, increased anxiety and reduced social interaction.

Tests showed that sperm from one of the modified monkeys could be used to produce offspring which also carried the MECP2 gene. These offspring also showed reduced social interaction.

Previous animal studies into ASD have mainly relied on rodents, so the hope is that the more human-like monkeys will provide a greater insight into the condition and possibly lead to new treatments.  

Where did the story come from?

The study was carried out by researchers from the Chinese Academy of Sciences and Fundan University. 

Funding was provided by the CAS Strategic Priority Research Program, the MoST 973 Program, NSFC grants, the National Key Technology R&D Program of China, and the Shanghai City Committee of Science and Technology Project.

The study was published in the peer-reviewed scientific journal Nature. The study can be read for free online, but you have to pay to download it.

Generally, this study has been reported accurately by the UK media, accompanied by an explanation of the potentially important role of monkeys in advancing medical research.


What kind of research was this?

This is an animal study on monkeys, with researchers looking at whether they could generate an animal model of ASD.

They did this by genetically modifying monkeys to carry a form of the human MECP2 gene that would be active in their brains. In humans, mutations in this gene cause Rett syndrome – a complex and severe condition, which includes autism spectrum behaviours. People who carry an extra copy of the gene also show symptoms of ASD. 

The researchers wanted to generate an animal model of ASD, so they could study the condition and possible treatments with greater ease. Making animal models of complex human conditions such as ASD is very difficult. However, it is hoped that they can give an early indication of whether a new drug or treatment might hold some promise for human use.

Animal studies are often used to study disease processes and treatments. 


What did the research involve?

This study genetically modified monkeys to carry a form of the MECP2 gene (called the "transgenic" group) which would be active in the monkeys' brains. The researchers compared the genetically modified monkeys with similarly aged non-genetically modified monkeys for the following behaviours:

  • movement
  • social interaction
  • behaviours when anxious – particularly sounds they made in response to human gaze, which the monkeys can find threatening
  • cognitive functions, including learning

The researchers also investigated whether the genetically modified monkeys could pass the human gene on to their offspring. If the monkeys did pass on the gene, the researchers could continue to study these transgenic monkeys' offspring without having to genetically modify new monkeys continuously.


What were the basic results?

It was found that the genetically modified monkeys showed some autism-like behaviours.

The transgenic monkeys spent more time moving in circular patterns than the non-genetically modified monkeys, despite their total time in motion being similar.

The response to the human gaze test found that the total number of anxiety-related grunts made by the transgenic monkeys was significantly higher than that of the non-genetically modified monkeys. Transgenic monkeys were also found to spend less time interacting socially.

The cognitive function tests showed similar findings in both groups of monkeys, including for learning.

The researchers also observed that it is possible for sperm from one of the transgenic monkeys to produce offspring which also carried human copies of the MECP2 gene. The offspring also showed reduced social interaction compared to the non-genetically modified monkeys.


How did the researchers interpret the results?

The researchers state that they were able to create monkeys with the human MECP2 gene. These monkeys showed autism-like behaviours, including an increased frequency of repetitive circular motion, increased anxiety and reduced social interaction.



This animal study genetically modified monkeys to carry the MECP2 gene to assess whether they would exhibit autism-like behaviours and pass this gene on to offspring. 

The researchers found that the modified monkeys did show some autism-like behaviours, namely an increase in repetitive circular motion, increased anxiety and reduced social interaction.

It has been welcomed by some experts in the field, who feel this is potentially very important and could allow greater understanding of autism. However, as mentioned, other experts have argued that while the research is impressive in terms of technical expertise, studying these types of monkeys may not provide any useful information about autism in humans.

Making animal models of complex human conditions such as ASD is very difficult. This is particularly true when we do not fully understand what causes the condition. In this case, the researchers have used genetic modification to mimic genetic changes in humans that are known to lead to autistic characteristics.

There will be differences between this newly developed animal model and ASD in people. However, researchers hope that studying the monkeys could help in understanding the condition better, and possibly give some early indication of whether new drugs might hold some promise for human use.

Links To The Headlines

Genetically modified monkeys created to help scientists study autism. The Guardian, January 25 2016

Chinese scientists create 'autistic' monkeys in controversial study they claim could lead to cure for humans. Mail Online, January 25 2016

Will creating monkeys with autism-like symptoms be any use? New Scientist, January 25 2016

Links To Science

Liu Z, Li X, Zhang J, et al. Autism-like behaviours and germline transmission in transgenic monkeys overexpressing MeCP2. Nature. Published online January 25 2016

Categories: NHS Choices

Zika virus: your questions answered

Mon, 25/01/2016 - 14:00

"Three Britons have contracted Zika virus – which may cause severe birth defects – after travelling to South and Central America," BBC News reports. So what is the Zika virus and what steps can you take to protect yourself? Answers below. 

What is the Zika virus?

The Zika virus is a mosquito-borne infection, which isn't harmful in most cases. However, it may be harmful for pregnancies, as it's been linked to birth defects – specifically, abnormally small heads (microcephaly).

It was first detected in the Zika forest of Uganda in 1947, but is now thought to have spread through most of South and Central America, and the Caribbean. The World Health Organization (WHO) has warned that the infection is likely to spread through the warmer regions of North America in the future.


What symptoms does the virus cause?

Many people don't have any symptoms. If symptoms do occur, they are usually mild and last around two to seven days. Commonly reported symptoms include:

  • a low-grade fever
  • joint pain (with possible swelling, mainly in the smaller joints of the hands and feet)
  • rash
  • conjunctivitis (red eyes)
  • headache
  • muscle pain
  • eye pain


How is the Zika virus diagnosed and treated?

The Zika virus can be diagnosed with a blood test.

There is no direct treatment for the symptoms of the Zika virus. Drinking plenty of water and taking paracetamol may help relieve symptoms. The use of aspirin or non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen is not recommended, as there is a potential risk they could trigger excessive bleeding.

If you still have symptoms after a week, you should seek medical advice.


What risks does the Zika virus pose in pregnancy?

There is evidence that pregnant women who contract the virus during pregnancy (at any trimester) have an increased risk of giving birth to a baby with an abnormally small head.

Current advice is that pregnant women should consider postponing travel to any region where a known outbreak of the Zika virus is occurring.

The WHO provides a regular updated bulletin about the current spread of the disease.


How does the Zika virus spread?

It is thought that most cases of the Zika virus are spread by infected mosquitoes biting humans. Unlike the mosquitoes that spread malaria, affected mosquitoes (the Aedes mosquito) are most active during the day.

The virus may also be spread during sexual intercourse.


How do I reduce my risk of contracting the Zika virus?

The most effective methods are to reduce your risk of being bitten by an Aedes mosquito. These include:

  • using insect repellent that contains N, N-diethyl-meta-toluamide (DEET) on exposed skin – the repellent is safe to use during pregnancy and should be applied to skin before sunscreen is applied
  • wearing loose clothing that covers your arms and legs 

Links To The Headlines

Zika virus: Outbreak 'likely to spread across Americas' says WHO. BBC News, January 23 2016

Zika virus: Three returning UK travellers diagnosed. The Guardian, January 23 2016

Three British travellers infected with Zika virus which has been linked to brain deformities in babies as expectant mothers warned not to travel to 22 affected countries. Mail Online, January 23 2016

Categories: NHS Choices

Playground equipment contains 'toxic levels of lead paint'

Mon, 25/01/2016 - 13:30

"Paint on playground equipment has been found to contain high amounts of the toxin lead – up to 40 times recommended levels," BBC News reports.

Researchers sampled levels at 26 playgrounds in the south of England and the results are worrying. Lead is well known to be a highly toxic metal and its use has been phased out over the years. Young children are particularly vulnerable to the effects of lead poisoning, which can affect both physical and mental development. Even small amounts of lead can be harmful.

As well as playgrounds, researchers also tested other public structures (272 in total) such as bridges and "traditional" telephone boxes.    

Lead was detected in the majority of all 272 public structures tested, and over a third had lead concentrations exceeding the recommended 5,000 micrograms per gram (mcg/g) limit.

The average level from all samples was around 1,000mcg/g, but some had levels up to around 100,000mcg/g. Also, it wasn't always those in a poor state of repair – some newly painted structures without visible flaking had levels exceeding the limit.

This study doesn't directly demonstrate any harms to children or people in general from touching these structures, but it does highlight an important concern for the public, and those involved in renovation and maintenance.

Encouraging your children to wash their hands after playing with playground facilities should help reduce the risk of any exposure.


Where did the story come from?

The study was carried out by two researchers from the School of Geography, Earth and Environmental Sciences, at Plymouth University. 

The study received partial funding from a Marine Institute grant from the university, and was published in the peer-reviewed scientific journal Science of the Total Environment.

The quality of the UK media's reporting of the study was mixed. While the overall findings of the study were reported accurately, many of the figures quoted do not correspond with the study. For example, the BBC says 50 playgrounds were tested, but the study only mentions 26 being tested.


What kind of research was this?

This was a cross sectional study that analysed the lead content in paint on a variety of structures in the urban and suburban environment of Plymouth. 

The toxicity of lead is well established, in particular its effect on the development of young children – the reason why the use of lead in products was phased out over several decades. However, previous research has documented that household paint particles contain various leaded pigments, causing paint to come under strict legislation. The US and other countries have set a limit for lead in consumer paints at 90 parts per million (ppm).

However, an environmental source that has received less attention is the paint used on external structures, particularly those where weather conditions lead to flaking paint. This study aimed to use a portable device – an X-ray fluorescence (FP-XRF) spectrometer – that would allow the researchers to analyse the paint content in a variety of structures in Plymouth.

This is a device that can accurately measure the amount and types of chemicals in an object.


What did the research involve?

The researchers visited 15 urban and suburban regions of Plymouth between February and April 2015. All visits were made in dry weather conditions. They examined as many painted public structures and facilities that they could access from roads or pavements, including gates, railings, post and telephone boxes and playground facilities.

They either assessed them with the FP-XRF spectrometer on site, or took samples from those that were visibly flaking for analysis in the laboratory. Overall they took 272 analyses – 58 on-site measurements and 224 paint fragments taken for laboratory analysis.


What were the basic results?

Lead was detected in 81% of all samples taken (221/272), with concentrations ranging from 20 to 389,000mcg/g of paint. The US safety limit of 5,000mcg/g was exceeded in just over a third (38%) of all of the samples analysed.  

Telephone boxes and bridges were the environmental structures with the most extensive paint flaking, and these structures had the highest lead concentrations. Their median (average) concentration was around 30-40,000mcg/g, and in 21 samples the lead exceeded 100,000mcg/g.

Looking at playgrounds specifically, 26 samples were analysed, and lead was detected in 20 of them. The average (median) lead concentration was 1,170mcg/g.

Lead was detected in all colours of paints, though levels were generally lower in grey/silver/white surfaces and higher in brown and red surfaces. 

Chromium – another toxic metal – was also detected in 106 of the samples.


How did the researchers interpret the results?

The researchers conclude: "Since the issues highlighted in the present study are neither likely to be restricted to this city, nor to the UK, a greater, general awareness and understanding of the sources and routes of exposure of exterior leaded paint is called for."



This research has analysed the lead content of a variety of painted public structures in the urban and suburban environment of Plymouth.

Though the research was not primarily intended to examine playground structures, as the researchers said: "Perhaps the greatest concerns arising from our research are the wide occurrence and high concentrations of lead in paints on public playground facilities."

Their tests included a variety of playground structures, such as roundabouts, climbing frames and monkey bars. Of the 26 samples measured, the average lead level was 1,170mcg/g, which is well below the recommended environmental limit of 5,000mcg/g. However, this average came from some playground samples with low levels (minimum 116mcg/g) and some with very high levels (maximum measured 115,000mcg/g).

The greatest risks are believed to be from older peeling paint on structures that children are in direct contact with, such as rails, swing or slide posts and climbing frames – particularly toddlers who are more likely to touch these surfaces and then put their hands to their mouths. However, as the researchers found, the highest levels don't necessarily always come from the oldest surfaces. One of the samples they took where lead levels exceeded 5,000mcg/g came from a range of facilities with generally intact paint that had been applied quite recently – date marked 2009.

The highest lead levels measured in the study came from bridges and telephone boxes – older structures in a poor state of repair. As the researchers suggest, the higher levels in these old structures may be the result of progressively newer paints containing less lead. 

However, the risk from these items wouldn't necessarily just be restricted to people touching these structures. Flakes of lead paint could contaminate soil, surface water and dust on roads and pavements. This could in theory result in lead particles being brought indoors on shoes and clothing.  

It is important to note, that while the potential that children or people in general could be at risk from touching painted external surfaces – or from bringing lead particles into the home – are highly plausible, they are not directly proven by this piece of research.

This study is also restricted to Plymouth, though as the researchers rightly say, there is no reason to suspect the findings would be limited to the environment of this city. Overall the findings are an important point of awareness for the public and those involved with the renovation, repair and maintenance of a wide variety of painted external structures. They also highlight the need for close regulation of the lead levels in paint. 

The best way to prevent your child being exposed to lead is to encourage them to always wash their hands after outside play and before eating. Regularly washing any of their toys or equipment they play with outside should also help. 

Links To The Headlines

Toxic paint levels at playgrounds, research suggests. BBC News, January 25 2016

Paint in children's playgrounds still contains dangerous levels of lead. The Daily Telegraph, January 25 2016

Harmful levels of lead in paint at dozens of playgrounds: Climbing frames, swings, slides and roundabouts among equipment contaminated. Mail Online, January 25 2016

Links To Science

Turner A, Solman KR. Lead in exterior paints from the urban and suburban environs of Plymouth, south west England. Science of the Total Environment. Published online January 2016

Categories: NHS Choices

Seasonal affective disorder 'may be a myth', study argues

Fri, 22/01/2016 - 12:00

"Stop blaming SAD for your bad mood – it doesn't exist! Seasonal changes have 'NO effect on depression,'' the Daily Mail reports.

Seasonal affective disorder (SAD) is described as a type of seasonal depression that may partly be triggered by reduced exposure to sunlight. This, in turn, can affect mood in a number of ways.

In this study, researchers took data from a telephone survey of around 35,000 people to see if season, latitude and sunlight exposure had a significant association with reported symptoms of depression. They did not find an association.

So does this mean SAD is a "myth", as some headlines claim? Not necessarily. A telephone survey is a very blunt tool and is no substitute for a face-to-face diagnosis by a trained clinician.

There is also, to some extent, a stigma attached to mental health problems, meaning some participants may not have provided entirely truthful answers. 

The important thing is if you are feeling depressed, whatever the time of year, seek medical advice from your GP.

SAD can be treated in the same way as depression, with talking therapies and medication. Some people have also reported benefiting from light box therapy, though the weight of evidence supporting this is relatively limited.  

Where did the story come from?

The study was carried out by researchers from Auburn University at Montgomery. No funding source or conflicts of interest were reported.

It was published in the peer-reviewed journal Clinical Psychological Science.

As is often the case, a single dissenting opinion has been overstated in the media as a change in expert consensus opinion.

SAD is recognised by bodies such as the Royal College of Psychiatrists and is included as a diagnosis in the American Psychiatric manual DSM-5.

Causes are likely to be multifactorial, rather than the oversimplification that the condition is caused by a reduction in sunlight exposure. 

What kind of research was this?

This was a cross-sectional study investigating SAD and whether there is a genuine link between exposure to sunlight and depressive symptoms. A number of analyses were conducted to assess this.

This type of study is not able to prove or disprove cause and effect.  

What did the research involve?

The researchers administered the Behavioural Risk Factor Surveillance System telephone survey to a random selection of the population in the United States.

This survey assesses health behaviours and collects information about health risk behaviours, healthcare access, and preventative measures.

The findings were analysed in a number of ways to draw links between sunlight exposure and depressive symptoms, including:

  • relationship of season
  • latitude or season
  • sunlight exposure

All models also assessed the effect of the following confounding variables:

  • age
  • race/ethnicity
  • gender
  • educational level
  • marital status
  • employment status

Classification of depression was made using an adaptation of the Patient Health Questionnaire depression scale (PHQ-8), a validated tool used to screen for symptoms of depression and give a rough guide to severity. The question about suicide was removed.  

What were the basic results?

The researchers analysed the surveys of 34,294 people with an average age of 52 years. There were 1,754 participants who were depressed, according to the PHQ-8 depression scale.

The researchers conducted their statistical models and found no effect of season, latitude or sunlight exposure on reported symptoms of depression.  

How did the researchers interpret the results?

The researchers concluded that, "Depression was unrelated to latitude, season, or sunlight. Results do not support the validity of a seasonal modifier in major depression.

"The idea of seasonal depression may be strongly rooted in folk psychology, but it is not supported by objective data. Consideration should be given to discontinuing seasonal variation as a diagnostic modifier of major depression." 


This cross-sectional study investigated whether season, latitude and sunlight exposure are linked to depressive symptoms that can be experienced in SAD.

The researchers found these factors had no effect on the occurrence of depressive symptoms.

However, this study has a number of important limitations. Depression was not a clinical diagnosis – it was based on the participant's response to a questionnaire over the phone.

This presents problems, as some people may not have answered questions truthfully, and those with depression or SAD may not have answered the phone.

The Royal College of Psychiatrists says around 3% of people will experience significant winter depression. This can be managed in the same way as clinical depression, through self-help techniques, talking therapies, medication, and the use of light box treatments.

Some of the self-help methods they suggest are:

  • increasing natural sunlight exposure, such as walking outside during daylight hours
  • regular exercise – read more about exercising in winter
  • recognising it is common to put on weight from eating more in autumn and winter, although excessive weight gain may make you feel worse – get tips on ways to avoid winter weight gain
  • connecting with others for mental wellbeing – sleepiness, lack of motivation, and irritability can be problematic, but gaining support from family and friends may help you manage these symptoms

Links To The Headlines

Stop blaming SAD for your bad mood - it doesn't exist! Seasonal changes have 'NO effect on depression'. Daily Mail, January 22 2016

Cheer up... seasonal depression exposed as a myth. The Times, January 22 2016 (subscription required)

You are just sad not SAD: Winter's blues is a total myth, according to an American study. The Sun, January 22 2016

Seasonal Affective Disorder is probably a myth, say psychologists. The Daily Telegraph, January 21 2016

SAD news: There's no such thing as seasonal affective disorder. Daily Express, January 21 2016

Links To Science

Traffanstedt MK, Mehta S, LoBello SG. Major Depression With Seasonal Variation - Is It a Valid Construct? Clinical Psychological Science. Published online January 19 2016

Categories: NHS Choices

Paternal depression linked to premature birth

Thu, 21/01/2016 - 14:00

"Depression in expectant fathers linked to premature births," The Independent reports. A Swedish study found a link between paternal depression occurring for the first time and an increased risk of very premature birth.

The study, which looked at 366,499 births, also confirmed that women with depression before or during pregnancy are more likely to have a premature birth (also known as a preterm birth).

However, the reasons for the association with depression are unclear. One theory for the link between premature birth and depression in women is that it may be caused by the treatment – antidepressants – rather than the illness.

Therefore, any effect of men having depression, the researchers suggest, may be more to do with the stressful effects that depression in a partner has on the pregnant woman.

This suggestion is supported by evidence that the risk of premature birth was absent in cases where the expectant father did not live with the mother.

The researchers also float the idea that antidepressants may have an effect on sperm, but conclude that this is unlikely.

A limitation of the study is that the diagnosis of depression was based on whether men were prescribed antidepressants. Antidepressants are also used for other conditions, such as anxiety disorders, so some of the diagnoses may have been incorrect.

Pregnancy can be a stressful time for both partners, so you shouldn’t feel guilty or ashamed if you do experience depression during this time. What is important is that you seek help by talking to your GP.


Where did the story come from?

The study was carried out by researchers from the Karolinska Institutet and Stockholm University, Sweden, and was funded by the Karolinksa Institutet. The study was published in the peer-reviewed journal BJOG: An international journal of obstetrics and gynaecology. It is published on an open-access basis, meaning it is free for anyone to read online.

The study was reported accurately in most of the UK media sources that covered it, although they did not point out a few weaknesses in the study that could make the results less reliable. For example, as mentioned, people were assumed to have depression if they were treated with antidepressants, although these are used for other conditions besides depression.


What kind of research was this?

This was a national cohort study, using data from the Medical Birth Register of Sweden. This type of study is good at finding links between factors – in this case, depression and preterm birth – but cannot prove that one causes the other.


What did the research involve?

Researchers used data from a big national registry to look at hundreds of thousands of births, including almost 17,000 preterm births. They used linked databases to see whether either parent had been treated for depression in the two years prior to conception or the first 24 weeks of the pregnancy. 

After adjusting their figures to take account of other factors that could influence the results, the researchers looked for links between depression in either parent and preterm birth. They assumed people had depression if they'd been prescribed antidepressants, or if they had received any treatment for depression in or out of hospital.

Other factors taken into account included the following confounders:

  • whether a woman had previously had a miscarriage or ectopic pregnancy
  • her height and weight
  • whether she smoked
  • her age
  • how many times she'd given birth

They also looked at pregnancy complications, including gestational diabetes and pre-eclampsia. For fathers, they considered age, years of education and household income.

The researchers checked their figures for the effects of previous pregnancy or birth problems, the effects of both partners having had depression, and the parents living together or apart. They looked separately at very early (22 to 31 weeks) and moderately early (32 to 36 weeks) births.

They also looked for differences between "new" episodes of depression (where someone had treatment for depression after a period of 12 months when they’d had no depression) or "recurrent" depression.

Finally, they calculated the effects of depression in both men and women, on the chances of very early and moderately early prematurity.


What were the basic results?

The study found that women with new episodes of depression had a 34% higher chance of a moderately preterm birth (odds ratio [OR] 1.34, 95% confidence interval [CI] 1.22 to 1.46), which increased to 42% with repeat depression (OR 1.42, 95% CI 1.32 to 1.53). However, the link between depression in woman and very preterm births was small enough that it could be down to chance. 

By contrast, new depression in men was linked to a 38% higher chance of very preterm birth (OR 1.38, 95% CI 1.04 to 1.83), but not to a moderately preterm birth. Repeat depression was not linked to preterm birth.


How did the researchers interpret the results?

The researchers concluded that "paternal depression around the time of conception and in early pregnancy can have an effect" on the mother and baby, and "can increase the risk of preterm birth". They suggest that this is because of the stress placed on the pregnant women if her partner is depressed, and the lack of social support she may get from a depressed partner. They suggest that paternal depression may also affect sperm quality, especially for very early birth.

They say that the lack of effect seen in men with repeated depression may mean that men who have had their depression recognised and treated before may place less stress on their partner than men with newly-recognised depression.

They point out the contrast in the results seen for men and women. Women with repeated depression had a stronger link with preterm birth, but only for moderately preterm deliveries. They say this suggests that the effect of treatment (antidepressants) may be more important than the effects of depression.



This study has found a link between depression in expectant fathers and an increased risk of preterm birth in their babies. It was based on large, independent sources of data, and the researchers adjusted their figures to take account of many factors that could have skewed the results.

However, it's worth noting a few uncertainties.

The main measure of depression was whether people took antidepressants. People take antidepressants for many reasons, including anxiety and chronic pain. Also, many people with depression don’t take antidepressants, and men in particular are less likely to come forward for any type of treatment. Some of the men thought to be healthy might have had undiagnosed depression.

Depression in men was only linked to prematurity in certain situations. After taking all other factors into consideration, the results were only statistically significant for new depression in very preterm births, not for repeat depression, or new depression in moderately preterm births. There were only 2,194 very pre-term births out of a total of 366,499, and the findings were only just statistically significant (as seen by the odds ratio of 1.04 to 1.83). This suggests the results may not be completely reliable.

It's also worth bearing in mind that the study cannot show that depression, in men or women, directly causes the increased chances of preterm birth. This type of study can never account for all the possible confounding factors that might have caused the results.

The researchers say their findings should be investigated with a trial of screening expectant fathers and treating them for depression. This would help us to discover whether the results hold true.

However, depression is a debilitating condition for men and women, which affects not just the person who has it, but their close family. It seems feasible that a pregnant woman whose partner is depressed will see an effect on her own health, and possibly that of her baby.

Depression is treatable, with talking therapies as well as antidepressants. Anyone who is worried they may be depressed should get help from their GP.

Links To The Headlines

Depression in expectant fathers linked to premature births. The Independent, January 20 2016

Depression in fathers-to-be linked to premature births. The Daily Telegraph, January 20 2016

Babies are more likely to be born premature if EITHER parent suffers depression during pregnancy. Mail Online, January 21 2016

Links To Science

Liu C, Cnattingius S, Bergström M, et al. Prenatal parental depression and preterm birth: a national cohort study. BJOG: An International Journal of Obstetrics & Gynaecology. Published online January 19 2016

Categories: NHS Choices

New genetic risk factor for ovarian cancer identified

Thu, 21/01/2016 - 13:30

"A faulty gene has been identified that increases the risk of ovarian cancer more than threefold," The Independent reports. The genetic mutation, found in the BRIP1 gene, adds to the known genetic warning signs for ovarian cancer.

Exactly what causes ovarian cancer is not known, but around 10% of ovarian cancers are thought to be the result of a faulty gene. However, previous research has shown defects in the BRCA1 and BRCA2 genes increase the risk of both ovarian and breast cancer.

In this study, the researchers looked at whether defects in genes associated with the repair of BRCA1 or BRCA2 DNA also increase the risk of ovarian cancer. The researchers used data from women with and without cancer to test for defects in a few different genes.

Based on the resulting data, they estimated the risk of ovarian cancer for women with the BRIP1 mutation was 3.4 times greater than that of the UK general population.

To put that figure in a wider context, 58 out of every 1,000 women with the BRIP1 gene mutation would be expected to develop the condition.

These findings are of interest, and provide a route for further research in the area to understand more about the possible causes of ovarian cancer – and hopefully lead to better prevention and treatment strategies. 

Where did the story come from?

The study was carried out by researchers from a number of institutions, including the University of Southern California and the University of Cambridge.

Funding was provided by Cancer Councils across Australia, Cancer Research UK, the Eve Appeal (The Oak Foundation), the Fred C. and Katherine B. Andersen Foundation, the US National Institutes for Health, the National Health & Medical Research Council of Australia, Cancer Australia, Roswell Park Cancer Institute Alliance Foundation, the UK Department of Health, the UK National Institute for Health Research, and the US Army Medical Research and Materiel Command.

It was published in the peer-reviewed Journal of the National Cancer Institute.

The study was actually made public in 2015. It seems the charity Cancer Research UK has successfully tried to make the findings headline news, as the study received very little publicity when it was first released.

The UK media has largely reported on the study accurately, with quotes from the study authors explaining the potential importance of these findings.

The Independent usefully puts the increased risk associated with the BRIP1 gene mutation into a wider context that most people can understand.

Simply reporting that the mutation "increases the risk of ovarian cancer threefold" means little to people if they don't know what the overall baseline risk is.

However, The Daily Telegraph overstated the findings by stating that, "Screening could prevent one in five ovarian cancer deaths".

The researchers clearly stated larger studies are required to confirm the results before this gene is used to inform clinical decision making. 

What kind of research was this?

This modelling study aimed to assess whether a mutation shortening BARD1, BRIP1, NBN and PALB2 genes are associated with an increased risk of ovarian cancer in populations of European origin. It is thought such mutations could stop cells repairing their DNA, leading to cancer. 

Defects in the genes BRAC1 and BRAC2 are already known to increase the risk of cancer. It's thought the mutations studied here may prevent these two genes repairing DNA, though this theory is in the early stages of research. 

What did the research involve?

This study used data from a number of case control studies, one ovarian cancer registry, one case series, and women from the UK Familial Ovarian Cancer Screening Study (UKFOCSS).

The UKFOCSS included women over the age of 35 with a lifetime risk of at least 10% based on their family history.

Statistical methods were used to test for an association between the risk of ovarian cancer and the presence of the mutation in each gene. 

What were the basic results?

Results were available for 3,236 participants with ovarian cancer and 3,341 women without cancer. Any of these genetic mutations were found in 1.6% of women in the ovarian cancer group, compared with 0.5% in the control group.

When looking at each gene separately, a higher number of BRIP1 mutations were found in participants with ovarian cancer (0.92%) than without (0.09%). However, no differences were observed between groups for BARD1, NBN1 or PALB2 genes.

The presence of the mutations was evaluated further using the UKFOCSS, with some similar findings. Genetic mutations were significantly higher for those with ovarian cancer than those without for BRIP1 and PALB2, but there were no significant differences between groups for BARD1 or NBN.

The risk of ovarian cancer for women with the BRIP1 mutation was estimated to be 3.4 times greater than that of the UK general population using data from a number of case control studies

How did the researchers interpret the results?

The researchers concluded that, "Deleterious germline mutations in BRIP1 are associated with a moderate increase in EOC [epithelial ovarian cancer] risk.

"These data have clinical implications for risk prediction and prevention approaches for ovarian cancer, and emphasise the critical need for risk estimates based on very large sample sizes before genes of moderate penetrance have clinical utility in cancer prevention." 


This study was designed to assess whether a mutation that shortens the BARD1, BRIP1, NBN and PALB2 genes is associated with an increased risk of ovarian cancer in women of European origin.

The cause of ovarian cancer is not known, but certain factors are known to increase risk, including age, the number of eggs the ovaries release, and whether someone in your family has had ovarian or breast cancer in the past.

Genetic mutations are thought to be the cause of 10% of ovarian cancers. Screening is only available for women who are at a high risk of developing the condition because of a strong family history or inheritance of a particular faulty gene.

The researchers believe this particular type of genetic mutation stops cells repairing their DNA, and this could then lead to cancer.

Participants with ovarian cancer were found to have a higher number of mutations in the BRIP1 gene. This difference was not seen for the other genes tested, however.

This study has some limitations, which the authors do acknowledge. The prevalence of the mutation may have been underestimated, as sequencing coverage was less than 100% for each gene in all samples.

The researchers were not able to detect all mutations using their strategy. And the number of women with the genetic defect in the sample was very small.

These findings are of interest, and provide a route for more research in the area to understand more about the possible causes of ovarian cancer.

There are a number of ways you can reduce your risk of ovarian cancer, including staying a healthy weight.

Anything that stops the process of ovulation can also help minimise your chances of developing ovarian cancer. This includes:

  • being pregnant
  • breastfeeding
  • taking the contraceptive pill
  • having a hysterectomy

If you have a strong family history of ovarian cancer, you may also wish to talk to your GP about the screening for genes associated with the condition. 

Links To The Headlines

Ovarian cancer: Women with defective gene 'at higher risk of developing disease'. The Independent, January 19 2016

Scientists discover faulty gene that makes a woman 'THREE times more likely to develop ovarian cancer'. Mail Online, January 19 2016

32,500 British women unknowingly carry deadly ovarian cancer gene. The Daily Telegraph, January 19 2016

Links To Science

Ramus SJ, Song H, Dicks E, et al. Germline Mutations in the BRIP1, BARD1, PALB2, and NBN Genes in Women With Ovarian Cancer. Journal of National Cancer Institute. Published online August 27 2015

Categories: NHS Choices